Modulator Fakultas Kedokteran Universitas Trisakti

Stroke Hemoragik

2009-02-15T16:35:00.001-08:00

A stroke is the rapidly developing loss of brain functions due to a disturbance in the blood vessels supplying blood to the brain. This can be due to ischemia (lack of blood supply) caused by thrombosis or embolism or due to a hemorrhage. As a result, the affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech or inability to see one side of the visual field.[1] In the past, stroke was referred to as cerebrovascular accident or CVA, but the term "stroke" is now preferred.

A stroke is a medical emergency and can cause permanent neurological damage, complications and death. It is the leading cause of adult disability in the United States and Europe. In the UK, it is the second most common cause of death, the first being heart attacks and third being cancer. It is the number two cause of death worldwide and may soon become the leading cause of death worldwide.[2] Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation.[3] High blood pressure is the most important modifiable risk factor of stroke.[1]

The traditional definition of stroke, devised by the World Health Organization in the 1970s,[4] is a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.[1] With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.[5]

A stroke is occasionally treated with thrombolysis ("clot buster"), but usually with supportive care (speech and language therapy, physiotherapy and occupational therapy) in a "stroke unit" and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins, and in selected patients with carotid endarterectomy and anticoagulation.[1]
Classification
A slice of brain from the autopsy of a person who suffered an acute middle cerebral artery (MCA) stroke

Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemia is due to interruption of the blood supply, while hemorrhage is due to rupture of a blood vessel or an abnormal vascular structure. 80% of strokes are due to ischemia; the remainder are due to hemorrhage. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start off as ischemic stroke.[1]

[edit] Ischemic stroke

Main article: Cerebral infarction

In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen: thrombosis (obstruction of a blood vessel by a blood clot forming locally), embolism (idem due to an embolus from elsewhere in the body, see below),[1] systemic hypoperfusion (general decrease in blood supply, e.g. in shock)[6] and venous thrombosis.[7] Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.[1][8]

There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.[9][10] The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).[11][1]

[edit] Hemorrhagic stroke

Main articles: Intracranial hemorrhage and intracerebral hemorrhage

CT scan showing an intracerebral hemorrhage.

Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous head injury). Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging hematoma (pooling of blood).[citation needed]

[edit] Signs and symptoms

Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases don't progress further. The symptoms depend on the area of the brain affected. The more extensive the area of brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms: in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.

[edit] Early recognition

Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. Sudden-onset face weakness, arm drift, and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke.[12] Proposed systems include FAST (face, arm and speech test),[13] the Los Angeles Prehospital Stroke Screen (LAPSS)[14] and the Cincinnati Prehospital Stroke Scale (CPSS).[15] Use of these scales is recommended by professional guidelines.[16]

For people referred to the emergency room, early recognition of stroke is deemed important as this can expedite diagnostic tests and treatments. A scoring system called ROSIER (recognition of stroke in the emergency room) is recommended for this purpose; it is based on features from the medical history and physical examination.[17][16]

[edit] Subtypes

If the area of the brain affected contains one of the three prominent Central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:

* hemiplegia and muscle weakness of the face
* numbness
* reduction in sensory or vibratory sensation

In most cases, the symptoms affect only one side of the body (unilateral). The defect in the brain is usually on the opposite side of the body (depending on which part of the brain is affected). However, the presence of any one of these symptoms does not necessarily suggest a stroke, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms.

In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting the brain stem therefore can produce symptoms relating to deficits in these cranial nerves:

* altered smell, taste, hearing, or vision (total or partial)
* drooping of eyelid (ptosis) and weakness of ocular muscles
* decreased reflexes: gag, swallow, pupil reactivity to light
* decreased sensation and muscle weakness of the face
* balance problems and nystagmus
* altered breathing and heart rate
* weakness in sternocleidomastoid muscle with inability to turn head to one side
* weakness in tongue (inability to protrude and/or move from side to side)

If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

* aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area)
* apraxia (altered voluntary movements)
* visual field defect
* memory deficits (involvement of temporal lobe)
* hemineglect (involvement of parietal lobe)
* disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
* anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)

If the cerebellum is involved, the patient may have the following:

* trouble walking
* altered movement coordination
* vertigo and or disequilibrium

[edit] Associated symptoms

Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain.

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

Causes
Thrombotic stroke

In thrombotic stroke, a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus". Thrombotic stroke can be divided into two types depending on the type of vessel the thrombus is formed on:

* Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia.
* Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery. Diseases that may form thrombi in the small vessels include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) and microatheroma (small atherosclerotic plaques).

Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.[18]

Embolic stroke

An embolic stroke refers to the blockage of an artery by an embolus, a travelling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).

Because an embolus arises from elsewhere, local therapy only solves the problem temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.

Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain.

Cardiac causes can be distinguished between high and low-risk:[19]

* High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of the atrium or vertricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction <28 percent, symptomatic congestive heart failure with ejection fraction <30 percent, dilated cardiomyopathy, Libman-Sacks endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myxoma and coronary artery bypass graft (CABG) surgery
* Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the ascending aorta or proximal arch

Systemic hypoperfusion

Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also referred to as "last meadow" to point to the fact that in irrigation the last meadow receives the least amount of water.

Venous thrombosis

Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.[7]

Intracerebral hemorrhage

It generally occurs in small arteries or arterioles and is commonly due to hypertension, trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g. amphetamines or cocaine), and vascular malformations. The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage.

[edit] Pathophysiology
Ischemic
Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after a few hours will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries. These break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels.

Due to collateral circulation, within the region of brain tissue affected by ischemia there is a spectrum of severity. Thus, part of the tissue may immediately die while other parts may only be injured and could potentially recover. The ischemia area where tissue might recover is referred to as the ischemic penumbra.

As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails leading to failure of energy dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.

Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling.[18]

These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs.

Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge Reactive oxygen species, inhibit apoptosis, or inhibit excitotoxic neurotransmitters, for example, have been shown experimentally to reduce tissue injury due to ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported be neuroprotective in stroke. This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results.[18]

In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.

As is the case with any type of brain injury, the immune system is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. Inhibition of the inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies.

[edit] Hemorrhagic

Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.[18]

[edit] Diagnosis

Stroke is diagnosed through several techniques: a neurological examination, CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no commonly used blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.[20]

[edit] Imaging

For diagnosing ischemic stroke in the emergency setting:[21]

* CT scans (without contrast enhancements)

sensitivity= 16%
specificity= 96%

* MRI scan

sensitivity= 83%
specificity= 98%

For diagnosing hemorrhagic stroke in the emergency setting:

* CT scans (without contrast enhancements)

sensitivity= 89%
specificity= 100%

* MRI scan

sensitivity= 81%
specificity= 100%

For detecting chronic hemorrhages, MRI scan is more sensitive.[22]

For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.

[edit] Underlying etiology

When a stroke has been diagnosed, various other studies may be performed to determine the underlying etiology. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. Commonly used techniques include:

* an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteries
* an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream)
* a Holter monitor study to identify intermittent arrhythmias
* an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)
* blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria

[edit] Prevention

Given the disease burden of stroke, prevention is an important public health concern.[23] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[23] Recent guidelines detail the evidence for primary prevention in stroke.[24] Because stroke may indicate underlying atherosclerosis, it is important to determine the patient's risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin prevents against first stroke in patients who have suffered a myocardial infarction.[25]

[edit] Risk factors

The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation. Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking[26][27] (active and passive), heavy alcohol consumption[28] and drug use,[29] lack of physical activity, obesity and unhealthy diet.[30] Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).[31] The drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-counter cough and cold drugs containing sympathomimetics.[32][33]

No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.[34] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[35] Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.

Blood pressure

Hypertension accounts for 35-50% of stroke risk.[36] Epidemiological studies suggest that even a small blood pressure reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer strokes.[37] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[38][39] It is equally important in secondary prevention.[40] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[41][42][43] Studies show that intensive antihypertensive therapy results in a greater risk reduction.[44] The available evidence does not show large differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection against other forms of cardiovascular disease should be considered and cost.[44][45]

Atrial fibrillation

Patients with atrial fibrillation have a risk of 5% each year to develop stroke, and this risk is even higher in those with valvular atrial fibrillation.[46] Depending on the stroke risk, anticoagulation with medications such as coumarins or aspirin is warranted for stroke prevention.[47]

Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke.[48][39] Statins have been shown to reduce the risk of stroke by about 15%.[49] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[50] statins might exert their effect through mechanisms other than their lipid-lowering effects.[49]

Diabetes mellitus

Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and hyperlipidemia. Intensive disease control has been shown to reduce microvascular complications such as nephropathy and retinopathy but not macrovascular complications such as stroke.[51][52]

Anticoagulation drugs

Oral anticoagulants such as warfarin have been the mainstay of stroke prevention for over 50 years. However, several studies have shown that aspirin and antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack. Low doses of aspirin (for example 75-150 mg) are as effective as high doses but have fewer side-effects; the lowest effective dose remains unknown.[53] Thienopyridines (clopidogrel, ticlopidine) are modestly more effective than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more expensive.[54] Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[54] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side-effect.[55] Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction.[25] > Oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.[56]

In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding.[57][58] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.[59][60]

Surgery

Surgical procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large body of evidence supporting this procedure in selected cases.[35] Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous symptomatic stroke.[61] Carotid artery stenting has not been shown to be equally useful.[62][63] Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.[35] Surgery is most efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.[64][65]

Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.[66] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.[67][68] To be beneficial, the complication rate of the surgery should be kept > 4%. Even then, for 100 surgeries, 5 patients will benefit by avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-free but would also have done so without intervention.[35]

Nutritional and metabolic interventions

Nutrition, specifically the Mediterranean-style diet, has the potential of more than halving stroke risk.[69]

With regards to lowering homocysteine, a meta-analysis of previous trials has concluded that lowering homocysteine with folic acid and other supplements may reduce stroke risk.[70] However, the two largest randomized controlled trials included in the meta-analysis had conflicting results. One reported positve results;[71] whereas the other was negative.[72]

[edit] Treatment

[edit] Stroke unit

Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in hospital staffed by nurses and therapists with experience in stroke. It has been shown that people admitted to a stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors with experience in stroke.[1]

When an acute stroke is suspected by history and physical examination, the goal of early assessment is to determine the cause. Treatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic. A non-contrast head CT scan can rapidly identify a hemorrhagic stroke by imaging bleeding in or around the brain. If no bleeding is seen, a presumptive diagnosis of ischemic stroke is made.

[edit] Treatment of ischemic stroke

Ischemic stroke is caused by a thrombus (blood clot) occluding blood flow to an artery supplying the brain. Definitive therapy is aimed at removing the blockage by breaking the clot, thrombolysis, or by removing it mechanically, thrombectomy. The more rapidly bloodflow is restored to the brain, the fewer brain cells die.[73]

Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. To this end, treatment with medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating.

In addition to definitive therapies, management of acute stroke includes control of blood sugars, ensuring the patient has adequate oxygenation and adequate intravenous fluids. Patients may be positioned with their heads flat on the stretcher, rather than sitting up, to increase blood flow to the brain. It is common for the blood pressure to be elevated immediately following a stroke. Although high blood pressure may cause some strokes, hypertension during acute stroke is desirable to allow adequate blood flow to the brain.

[edit] Thrombolysis

In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. However, the use of tPA in acute stroke is controversial. On one hand, it is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or recent surgery). This position for tPA is based upon the findings of two studies by one group of investigators[74] which showed that tPA improves the chances for a good neurological outcome. When administered within the first three hours, 39% of all patients who were treated with tPA had a good outcome at three months, only 26% of placebo controlled patients had a good functional outcome. A recent study using alteplase for thrombolysis in ischemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset. [75] However, in the NINDS trial 6.4% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. tPA is often misconstrued as a "magic bullet" and it is important for patients to be aware that despite the study that supports its use, some of the data were flawed and the safety and efficacy of tPA is controversial. A recent study found the mortality to be higher among patients receiving tPA versus those who did not.[76] Additionally, it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.[77]

[edit] Mechanical thrombectomy
Merci Retriever L5.

Another intervention for acute ischemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective,[78][79][80][81] though no differences have been found between newer and older versions of the devices.[82] The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.

[edit] Therapeutic hypothermia

Main article: therapeutic hypothermia

Most of the data concerning therapeutic hypothermia’s effectiveness in treating ischemic stroke is limited to animal studies. These studies have focused primarily on ischemic as opposed to hemorrhagic stroke, as hypothermia has been associated with a lower clotting threshold. In these animal studies investigating the effect of temperature decline following ischemic stroke, hypothermia has been shown to be an effective all purpose neuroprotectant.[83]This promising data has lead to the initiation of a variety of human studies. Unfortunately, at the time of this article’s publishing, this research have yet to return results. However, in terms of feasibility, the use of hypothermia to control intracranial pressure (ICP) after an ischemic stroke was found to be both safe and practical. The device used in this study was called the Arctic Sun[84]

[edit] Secondary prevention of ischemic stroke

Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.[85]. However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.[86] Stroke prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system.

If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.

[edit] Treatment of hemorrhagic stroke

Patients with intracerebral hemorrhage require neurosurgical evaluation to detect and treat the cause of the bleeding, although many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.

[edit] Care and rehabilitation

Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role.

A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include nursing staff, physiotherapy, occupational therapy, speech and language therapy, and usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one third of the patients manifest post stroke depression. Validated instruments such as the Barthel scale may be used to assess the likelihood of a stroke patient being able to manage at home with or without support subsequent to discharge from hospital.

Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.

For most stroke patients, physical therapy (PT) and occupational therapy (OT) are the cornerstones of the rehabilitation process, but in many countries Neurocognitive Rehabilitation is used. Often, assistive technology such as a wheelchair, walkers, canes, and orthosis may be beneficial. PT and OT have overlapping areas of working but their main attention fields are; PT involves re-learning functions as transferring, walking and other gross motor functions. OT focusses on exercises and training to help relearn everyday activities known as the Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding speech or written words, problems forming speech and problems with swallowing.

Patients may have particular problems, such as complete or partial inability to swallow, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.

Stroke rehabilitation should be started as immediately as possible and can last anywhere from a few days to over a year. Most return of function is seen in the first few days and weeks, and then improvement falls off with the "window" considered officially by U.S. state rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily rehabilitation exercises should continue to be part of the stroke patient's routine. Complete recovery is unusual but not impossible and most patients will improve to some extent : a correct diet and exercise are known to help the brain to self-recover.

[edit] Prognosis
Disability affects 75% of stroke survivors enough to decrease their employability.[87] Stroke can affect patients physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.[88] Dysfunctions correspond to areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include paralysis, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.

Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.

30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.[89] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.

Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient's actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion.[87] Some patients show the opposite of what they feel, for example crying when they are happy.[90] Emotional lability occurs in about 20% of stroke patients.

Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.

Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.[91][92]

[edit] Epidemiology

Stroke could soon be the most common cause of death worldwide.[93] Stroke is currently the second leading cause of death in the Western world, ranking after heart disease and before cancer,[1] and causes 10% of deaths worldwide.[94] Geographic disparities in stroke incidence have been observed, including the existence of a "stroke belt" in the southeastern United States, but causes of these disparities have not been explained.

The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.[95] Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.[89][18] A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in fetuses.

Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time.[96] The results of this study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases one's risk of future strokes.

Men are 1.25 times more likely to suffer strokes than women,[18] yet 60% of deaths from stroke occur in women.[90] Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[18] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).

[edit] History
Hippocrates first described the sudden paralysis that is often associated with stroke.

Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis. Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon.[97][98]

The word stroke was used as a synonym for apoplectic seizure as early as 1599,[99] and is a fairly literal translation of the Greek term.

In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains.[97][18] Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke when he suggested that apoplexy might be caused by a blockage to those vessels.[18]

Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[100]

Gangguan Gizi

2009-02-15T16:29:00.000-08:00

BAB I

PENDAHULUAN

A. LATAR BELAKANG

Anak usia di bawah lima tahun (balita) merupakan kelompok yang rentan terhadap kesehatan dan gizi. Kurang Energi Protein (KEP) adalah salah satu masalah gizi utama yang banyak dijumpai pada balita di Indonesia. Dalam Repelita VI, pemerintah dan masyarakat berupaya menurunkan prevalensi KEP dari 40% menjadi 30%. Namun saat ini di Indonesia sedang dilanda krisis ekonomi yang berdampak juga pada status gizi balita, dan diasumsi kecenderungan kasus KEP berat/gizi buruk akan bertambah.

Untuk mengantisipasi masalah tersebut diperlukan kesiapan dan pemberdayaan tenaga kesehatan dalam mencegah dan menanggulangi KEP berat/gizi buruk secara terpadu ditiap jenjang administrasi, termasuk kesiapan sarana pelayanan kesehatan seperti Rumah Sakit Umum, Puskesmas perawatan, puskesmas, balai pengobatan (BP), puskesmas pembantu, dan posyandu/PPG (Pusat Pemulihan Gizi).

Agar upaya penanggulangan KEP di puskesmas dan rumah tangga dapat mencapai sasaran yang diharapkan secara optimal diperlukan adanya Buku Pedoman sebagai acuan.

B. PENGERTIAN, KLASIFIKASI DAN GEJALA KLINIS KURANG ENERGI PROTEIN

1. Pengertian Kurang Energi Protein (KEP)

KEP adalah keadaan kurang gizi yang disebabkan oleh rendahnya konsumsi energi dan protein dalam makanan sehari-hari sehingga tidak memenuhi Angka Kecukupan Gizi (AKG).

2. Klasifikasi KEP

Untuk tingkat puskesmas penentuan KEP yang dilakukan dengan menimbang BB anak dibandingkan dengan umur dan menggunakan KMS dan Tabel BB/U Baku Median WHO-NCHS (lampiran 1)

2.1.KEP ringan bila hasil penimbangan berat badan pada KMS terletak pada pita warna kuning

2.2.KEP sedang bila hasil penimbangan berat badan pada KMS terletak di Bawah Garis Merah (BGM).

2.3.KEP berat/gizi buruk bila hasil penimbangan BB/U <60% baku median WHO-NCHS. Pada KMS tidak ada garis pemisah KEP berat/Gizi buruk dan KEP sedang, sehingga untuk menentukan KEP berat/gizi buruk digunakan Tabel BB/U Baku Median WHO-NCHS (lampiran 1)

3. Gejala klinis Balita KEP berat/Gizi buruk

Untuk KEP ringan dan sedang, gejala klinis yang ditemukan hanya anak tampak kurus. Gejala klinis KEP berat/gizi buruk secara garis besar dapat dibedakan sebagai marasmus, kwashiorkor atau marasmic-kwashiorkor. Tanpa mengukur/melihat BB bila disertai edema yang bukan karena penyakit lain adalah KEP berat/Gizi buruk tipe kwasiorkor.

a. Kwashiorkor

o Edema, umumnya seluruh tubuh, terutama pada punggung kaki (dorsum pedis)
o Wajah membulat dan sembab
o Pandangan mata sayu
o Rambut tipis, kemerahan seperti warna rambut jagung, mudah dicabut tanpa rasa sakit, rontok
o Perubahan status mental, apatis, dan rewel
o Pembesaran hati
o Otot mengecil (hipotrofi), lebih nyata bila diperiksa pada posisi berdiri atau duduk
o Kelainan kulit berupa bercak merah muda yang meluas dan berubah warna menjadi coklat kehitaman dan terkelupas (crazy pavement dermatosis)
o Sering disertai : • penyakit infeksi, umumnya akut

· anemia

· diare.

2. Marasmus:

- Tampak sangat kurus, tinggal tulang terbungkus kulit

- Wajah seperti orang tua

- Cengeng, rewel

- Kulit keriput, jaringan lemak subkutis sangat sedikit sampai tidak ada (baggy pant/pakai celana longgar)

o Perut cekung
o Iga gambang

- Sering disertai: - penyakit infeksi (umumnya kronis berulang)

- diare kronik atau konstipasi/susah buang air

3. Marasmik-Kwashiorkor:

- Gambaran klinik merupakan campuran dari beberapa gejala klinik Kwashiorkor dan Marasmus, dengan BB/U <60% baku median WHO-NCHS disertai edema yang tidak mencolok.

SEMUA PENDERITA KEP BERAT
UMUMNYA

DISERTAI DENGAN ANEMIA DAN DEFISIENSI MIKRONUTRIEN LAIN

3. PENEMUAN KASUS

Penemuan kasus balita KEP dapat dimulai dari :

1. Posyandu/Pusat Pemulihan Gizi

Pada penimbangan bulanan di posyandu dapat diketahui apakah anak balita berada pada daerah pita warna hijau, kuning, atau dibawah garis merah (BGM).

Bila hasil penimbangan BB balita dibandingkan dengan umur di KMS terletak pada pita kuning, dapat dilakukan perawatan di rumah , tetapi bila anak dikategorikan dalam KEP sedang-berat/BGM, harus segera dirujuk ke Puskesmas.

2. Puskesmas

Apabila ditemukan BB anak pada KMS berada di bawah garis merah (BGM) segera lakukan penimbangan ulang dan kaji secara teliti. Bila KEP Berat/Gizi buruk (BB < 60% Standard WHO-NCHS) lakukan pemeriksaan klinis dan bila tanpa penyakit penyerta dapat dilakukan rawat inap di puskesmas. Bila KEP berat/Gizi buruk dengan penyakit penyerta harus dirujuk ke rumah sakit umum.

Semua balita yang datang ke Puskesmas harus ditentukan status gizinya

ANAK DENGAN TANDA-TANDA KLINIS
KEP BERAT/GIZI BURUK

(MARASMUS,KWASHIORKOR, MARASMIC KWASHIORKOR)
HARUS DI RAWAT INAP
BAB II
MEKANISME PELAYANAN GIZI
BALITA KEP BERAT/GIZI BURUK

A. Tingkat Rumah Tangga

o Ibu membawa anak untuk ditimbang di posyandu secara teratur setiap bulan untuk mengetahui pertumbuhan berat badannya
o Ibu memberikan hanya ASI kepada bayi usia 0-4 bulan
o Ibu tetap memberikan ASI kepada anak sampai usia 2 tahun
o Ibu memberikan MP-ASI sesuai usia dan kondisi kesehatan anak sesuai anjuran pemberian makanan (lampiran 5)
o Ibu memberikan makanan beraneka ragam bagi anggauta keluarga lainnya
o Ibu segera memberitahukan pada petugas kesehatan/kader bila balita mengalami sakit atau gangguan pertumbuhan
o Ibu menerapkan nasehat yang dianjurkan petugas

B. Tingkat Posyandu

- Kader melakukan penimbangan balita setiap bulan di posyandu serta mencatat hasil penimbangan pada KMS

o Kader memberikan nasehat pada orang tua balita untuk memberikan hanya ASI kepada bayi usia 0-4 bulan dan tetap memberikan ASI sampai usia 2 tahun
o Kader memberikan penyuluhan pemberian MP-ASI sesuai dengan usia anak dan kondisi anak sesuai kartu nasehat ibu
o Kader menganjurkan makanan beraneka ragam untuk anggauta keluarga lainnya
o Bagi balita dengan berat badan tidak naik (“T”) diberikan penyuluhan gizi seimbang dan PMT Penyuluhan
o Kader memberikan PMT-Pemulihan bagi balita dengan berat badan tidak naik 3 kali (“3T”) dan berat badan di bawah garis merah (BGM)
o Kader merujuk balita ke puskesmas bila ditemukan gizi buruk dan penyakit penyerta lain
o Kader melakukan kunjungan rumah untuk memantau perkembangan kesehatan balita

3. Pusat pemulihan Gizi (PPG)

PPG merupakan suatu tempat pelayanan gizi kepada masyarakat yang ada di desa dan dapat dikembangkan dari posyandu. Pelayanan gizi di PPG difokuskan pada pemberian makanan tambahan pemulihan bagi balita KEP. Penanganan PPG dilakukan oleh kelompok orang tua balita (5-9 balita) yang dibantu oleh kader untuk menyelenggarakan PMT Pemulihan anak balita.

Layanan yang dapat diberikan adalah :

o Balita KEP berat/gizi buruk yang tidak menderita penyakit penyerta lain dapat dilayani di PPG
o Kader memberikan penyuluhan gizi /kesehatan serta melakukan demonstrasi cara menyiapkan makanan untuk anak KEP berat/gizi buruk
o Kader menimbang berat badan anak setiap 2 minggu sekali untuk memantau perubahan berat badan dan mencatat keadaan kesehatannya

o Bila anak berat badan nya tidak naik atau tetap maka berikan penyuluhan gizi seimbang untuk dilaksanakan di rumah
o Bila anak sakit dianjurkan untuk memeriksakan anaknya ke puskesmas

o Apabila berat badan anak berada di pita warna kuning atau di bawah garis merah (BGM) pada KMS, kader memberikan PMT Pemulihan
o Makanan tambahan diberikan dalam bentuk makanan jadi dan diberikan setiap hari.
o Bila makanan tidak memungkinkan untuk dimakan bersama, makanan tersebut diberikan satu hari dalam bentuk matang selebihnya diberikan dalam bentuk bahan makanan mentah
o Apabila berat badan anak berada di pita warna kuning pada KMS teruskan pemberian PMT pemulihan sampai 90 hari
o Apabila setelah 90 hari, berat badan anak belum berada di pita warna hijau pada KMS kader merujuk anak ke puskesmas untuk mencari kemungkinan penyebab lain
o Apabila berat badan anak berada di pita warna hijau pada KMS, kader menganjurkan pada ibu untuk mengikuti pelayanan di posyandu setiap bulan dan tetap melaksanakan anjuran gizi dan kesehatan yang telah diberikan
o Ibu memperoleh penyuluhan gizi/kesehatan serta demontrasi cara menyiapkan makanan untuk anak KEP
o Kader menganjurkan pada ibu untuk tetap melaksanakan nasehat yang diberikan tentang gizi dan kesehatan
o Kader melakukan kunjungan rumah untuk memantau perkembangan kesehatan dan gizi anak

4. Puskesmas

o Puskesmas menerima rujukan KEP Berat/Gizi buruk dari posyandu dalam wilayah kerjanya serta pasien pulang dari rawat inap di rumah sakit
o Menyeleksi kasus dengan cara menimbang ulang dan dicek dengan Tabel BB/U Baku Median WHO-NCHS (lampiran 1)
o Apabila ternyata berat badan anak berada di bawah garis merah (BGM) dianjurkan kembali ke PPG/posyandu untuk mendapatkan PMT pemulihan
o Apabila anak dengan KEP berat/gizi buruk (BB < 60% Tabel BB/U Baku Median WHO-NCHS) tanpa disertai komplikasi, anak dapat dirawat jalan di puskesmas sampai berat badan nya mulai naik 0,5 Kg selama 2 minggu dan mendapat PMT-P dari PPG
o Apabila setelah 2 minggu berat badannya tidak naik, lakukan pemeriksaan untuk evaluasi mengenai asupan makanan dan kemungkinan penyakit penyerta, rujuk ke rumah sakit untuk mencari penyebab lain
o Anak KEP berat/Gizi Buruk dengan komplikasi serta ada tanda-tanda kegawatdaruratan segera dirujuk ke rumah sakit umum
o Tindakan yang dapat dilakukan di puskesmas pada anak KEP berat/ gizi buruk tanpa komplikasi
o Memberikan penyuluhan gizi dan konseling diet KEP berat/Gizi buruk (dilakukan di pojok gizi)
o Melakukan pemeriksaan fisik dan pengobatan minimal 1 kali per minggu
o Melakukan evaluasi pertumbuhan berat badan balita gizi buruk setiap dua minggu sekali
o Melakukan peragaan cara menyiapkan makanan untuk KEP berat/Gizi buruk
o Melakukan pencatatan dan pelaporan tentang perkembangan berat badan dan kemajuan asupan makanan
o Untuk keperluan data pemantauan gizi buruk di lapangan, posyandu, dan puskesmas diperlukan laporan segera jumlah balita KEP berat/gizi buruk ke Dinas kesehatan kabupaten/kota dalam 24 jam dengan menggunakan formulir W1 dan laporan mingguan dengan menggunakan formulir W2 (lampiran 2)

o Apabila berat badan anak mulai naik, anak dapat dipulangkan dan dirujuk ke posyandu/PPG serta dianjurkan untuk pemantauan kesehatan setiap bulan sekali

o Petugas kesehatan memberikan bimbingan terhadap kader untuk melakukan pemantauan keadaan balita pada saat kunjungan rumah

BAB III

TATA LAKSANA
PELAYANAN KEP BERAT/GIZI BURUK
DI PUSKESMAS

A. PRINSIP DASAR PELAYANAN RUTIN KEP BERAT/GIZI BURUK

Pelayanan rutin yang dilakukan di puskesmas berupa 10 langkah penting yaitu:

1. Atasi/cegah hipoglikemia

2. Atasi/cegah hipotermia

3. Atasi/cegah dehidrasi

4. Koreksi gangguan keseimbangan elektrolit

5. Obati/cegah infeksi

6. Mulai pemberian makanan
7. Fasilitasi tumbuh-kejar (catch up growth)
8. Koreksi defisiensi nutrien mikro

9. Lakukan stimulasi sensorik dan dukungan emosi/mental

10. Siapkan dan rencanakan tindak lanjut setelah sembuh.

Dalam proses pelayanan KEP berat/Gizi buruk terdapat 3 fase yaitu fase stabilisasi, fase transisi, dan fase rehabilitasi. Petugas kesehatan harus trampil memilih langkah mana yang sesuai untuk setiap fase.

Tata laksana ini digunakan pada pasien Kwashiorkor, Marasmus maupun Marasmik-Kwashiorkor.

Bagan dan jadwal pengobatan sebagai berikut:

No FASE STABILISASI TRANSISI REHABILITASI
Hari ke 1-2 Hari ke 2-7 Minggu ke-2 Minggu ke 3-7

1 Hipoglikemia

2 Hipotermia

3 Dehidrasi

4 Elektrolit

5 Infeksi

6 MulaiPemberian

makanan

7 Tumbuh kejar

(Meningkatkan

Pemberian Makanan)

8 Mikronutrien Tanpa Fe dengan Fe

9 Stimulasi

10 Tindak lanjut

B. SEPULUH LANGKAH UTAMA PADA TATA LAKSANA KEP BERAT/GIZI BURUK

1. Pengobatan atau pencegahan hipoglikemia (kadar gula dalam darah rendah)

Hipoglikemia merupakan salah satu penyebab kematian pada anak dengan KEP berat/Gizi buruk. Pada hipoglikemia, anak terlihat lemah, suhu tubuh rendah. Jika anak sadar dan dapat menerima makanan usahakan memberikan makanan saring/cair 2-3 jam sekali. Jika anak tidak dapat makan (tetapi masih dapat minum) berikan air gula dengan sendok. Jika anak mengalami gangguan kesadaran, berikan infus cairan glukosa dan segera rujuk ke RSU kabupaten.

2. Pengobatan dan pencegahan hipotermia (suhu tubuh rendah)

Hipotermia ditandai dengan suhu tubuh yang rendah dibawah 360 C. Pada keadaan ini anak harus dihangatkan. Cara yang dapat dilakukan adalah ibu atau orang dewasa lain mendekap anak di dadanya lalu ditutupi selimut (Metode Kanguru). Perlu dijaga agar anak tetap dapat bernafas.

Cara lain adalah dengan membungkus anak dengan selimut tebal, dan meletakkan lampu didekatnya. Lampu tersebut tidak boleh terlalu dekat apalagi sampai menyentuh anak. Selama masa penghangatan ini dilakukan pengukuran suhu anak pada dubur (bukan ketiak) setiap setengah jam sekali. Jika suhu anak sudah normal dan stabil, tetap dibungkus dengan selimut atau pakaian rangkap agar anak tidak jatuh kembali pada keadaan hipothermia.

Tidak dibenarkan

penghangatan anak dengan menggunakan

botol berisi air panas

3. Pengobatan dan Pencegahan kekurangan cairan

Tanda klinis yang sering dijumpai pada anak penderita KEP berat/Gizi buruk dengan dehidrasi adalah :

· Ada riwayat diare sebelumnya

· Anak sangat kehausan

· Mata cekung

· Nadi lemah

· Tangan dan kaki teraba dingin

· Anak tidak buang air kecil dalam waktu cukup lama.

Tindakan yang dapat dilakukan adalah :

o Jika anak masih menyusui, teruskan ASI dan berikan setiap setengah jam sekali tanpa berhenti. Jika anak masih dapat minum, lakukan tindakan rehidrasi oral dengan memberi minum anak 50 ml (3 sendok makan) setiap 30 menit dengan sendok. Cairan rehidrasi oral khusus untuk KEP disebut ReSoMal (lampiran 4).
o Jika tidak ada ReSoMal untuk anak dengan KEP berat/Gizi buruk dapat menggunakan oralit yang diencerkan 2 kali. Jika anak tidak dapat minum, lakukankan rehidrasi intravena (infus) cairan Ringer Laktat/Glukosa 5 % dan NaCL dengan perbandingan 1:1.

KEP BERAT/GIZI BURUK YANG DIRUJUK KE RSU HARUS DILAKUKAN TINDAKAN PRA RUJUKAN UNTUK

MENGATASI HIPOGLIKEMI, HIPOTERMIA, DAN DEHIDRASI

4. Lakukan pemulihan gangguan keseimbangan elektrolit

Pada semua KEP berat/Gizi buruk terjadi gangguan keseimbangan elektrolit diantaranya :

o Kelebihan natrium (Na) tubuh, walaupun kadar Na plasma rendah.
o Defisiensi kalium (K) dan magnesium (Mg)

Ketidakseimbangan elektrolit ini memicu terjadinya edema dan, untuk pemulihan keseimbangan elektrolit diperlukan waktu paling sedikit 2 minggu.

JANGAN OBATI EDEMA DENGAN PEMBERIAN DIURETIKA

Berikan :

o Makanan tanpa diberi garam/rendah garam
o Untuk rehidrasi, berikan cairan oralit 1 liter yang diencerkan 2 X (dengan penambahan 1 liter air) ditambah 4 gr KCL dan 50 gr gula atau bila balita KEP bisa makan berikan bahan makanan yang banyak mengandung mineral ( Zn, Cuprum, Mangan, Magnesium, Kalium) dalam bentuk makanan lumat/lunak

Contoh bahan makanan sumber mineral

Sumber Zink : daging sapi, hati, makanan laut, kacang tanah,

telur ayam

Sumber Cuprum : daging, hati.

Sumber Mangan : beras, kacang tanah, kedelai.

Sumber Magnesium : kacang-kacangan, bayam.

Sumber Kalium : jus tomat, pisang, kacang2an, apel, alpukat,

bayam, daging tanpa lemak.

5. Lakukan Pengobatan dan pencegahan infeksi

Pada KEP berat/Gizi buruk, tanda yang umumnya menunjukkan adanya infeksi seperti demam seringkali tidak tampak, oleh karena itu pada semua KEP berat/Gizi buruk secara rutin diberikan antibiotik spektrum luas dengan dosis sebagai berikut :

UMUR

ATAU

BERAT BADAN
KOTRIMOKSASOL

(Trimetoprim + Sulfametoksazol)
o Beri 2 kali sehari selama 5 hari
AMOKSISILIN
o Beri 3 kali sehari untuk 5 hari
Tablet dewasa

80 mg trimeto

prim + 400 mg sulfametok

sazol
Tablet Anak

20 mg trimeto

prim + 100 mg sulfametok

sazol
Sirup/5ml

40 mg trimeto

prim + 200 mg sulfametok

sazol
Sirup

125 mg

per 5 ml
2 sampai 4 bulan

(4 - < 6 kg)

¼
1
2,5 ml
2,5 ml
4 sampai 12 bulan

(6 - < 10 Kg)

½
2
5 ml
5 ml
12 bln s/d 5 thn

(10 - < 19 Kg)

1
3
7,5 ml
10 ml

Vaksinasi Campak bila anak belum diimunisasi dan umur sudah mencapai 9 bulan

Catatan :

o Mengingat pasien KEP berat/Gizi buruk umumnya juga menderita penyakit infeksi, maka lakukan pengobatan untuk mencegah agar infeksi tidak menjadi lebih parah. Bila tidak ada perbaikan atau terjadi komplikasi rujuk ke Rumah Sakit Umum.

o Diare biasanya menyertai KEP berat/Gizi buruk, akan tetapi akan berkurang dengan sendirinya pada pemberian makanan secara hati-hati. Berikan metronidasol 7,5 mg/Kgbb setiap 8 jam selama 7 hari. Bila diare berlanjut segera rujuk ke rumah sakit

BILA DIARE BERLANJUT ATAU MEMBURUK

ANAK SEGERA DIRUJUK KE RUMAH SAKIT

6. Pemberian makanan balita KEP berat/Gizi buruk

Pemberian diet KEP berat/Gizi buruk dibagi dalam 3 fase, yaitu :

Fase Stabilisasi, Fase Transisi, Fase Rehabilitasi

Fase Stabilisasi ( 1-2 hari)

Pada awal fase stabilisasi perlu pendekatan yang sangat hati-hati, karena keadaan faali anak sangat lemah dan kapasitas homeostatik berkurang.

Pemberian makanan harus dimulai segera setelah anak dirawat dan dirancang sedemikian rupa sehingga energi dan protein cukup untuk memenuhi metabolisma basal saja.

Formula khusus seperti Formula WHO 75/modifikasi/Modisco ½ yang dianjurkan dan jadwal pemberian makanan harus disusun sedemikian rupa agar dapat mencapai prinsip tersebut diatas dengan persyaratan diet sebagai berikut :

o Porsi kecil, sering, rendah serat dan rendah laktosa
o Energi : 100 kkal/kg/hari
o Protein : 1-1.5 gr/kg bb/hari
o Cairan : 130 ml/kg bb/hari (jika ada edema berat 100 ml/Kg bb/hari)
o Bila anak mendapat ASI teruskan , dianjurkan memberi Formula WHO 75/pengganti/Modisco ½ dengan menggunakan cangkir/gelas, bila anak terlalu lemah berikan dengan sendok/pipet
o Pemberian Formula WHO 75/pengganti/Modisco ½ atau pengganti dan jadwal pemberian makanan harus disusun sesuai dengan kebutuhan anak

Keterangan :

o Pada anak dengan selera makan baik dan tidak edema, maka tahapan pemberian formula bisa lebih cepat dalam waktu 2-3 hari (setiap 2 jam)
o Bila pasien tidak dapat menghabiskan Formula WHO 75/pengganti/Modisco ½ dalam sehari, maka berikan sisa formula tersebut melalui pipa nasogastrik ( dibutuhkan ketrampilan petugas )
o Pada fase ini jangan beri makanan lebih dari 100 Kkal/Kg bb/hari
o Pada hari 3 s/d 4 frekwensi pemberian formula diturunkan menjadi setiap jam dan pada hari ke 5 s/d 7 diturunkan lagi menjadi setiap 4 jam
o Lanjutkan pemberian makan sampai hari ke 7 (akhir minggu 1)

Pantau dan catat :

o Jumlah yang diberikan dan sisanya
o Banyaknya muntah
o Frekwensi buang air besar dan konsistensi tinja
o Berat badan (harian)

- selama fase ini diare secara perlahan berkurang pada penderita dengan edema , mula-mula berat badannya akan berkurang kemudian berat badan naik

7. Perhatikan masa tumbuh kejar balita (catch- up growth)

Pada fase ini meliputi 2 fase yaitu fase transisi dan fase rehabilitasi :

Fase Transisi (minggu ke 2)

o Pemberian makanan pada fase transisi diberikan secara berlahan-lahan untuk menghindari risiko gagal jantung, yang dapat terjadi bila anak mengkonsumsi makanan dalam jumlah banyak secara mendadak.
o Ganti formula khusus awal (energi 75 Kkal dan protein 0.9-1.0 g per 100 ml) dengan formula khusus lanjutan (energi 100 Kkal dan protein 2.9 gram per 100 ml) dalam jangka waktu 48 jam. Modifikasi bubur/makanan keluarga dapat digunakan asalkan dengan kandungan energi dan protein yang sama.
o Kemudian naikkan dengan 10 ml setiap kali, sampai hanya sedikit formula tersisa, biasanya pada saat tercapai jumlah 30 ml/kgbb/kali pemberian (200 ml/kgbb/hari).

Pemantauan pada fase transisi:

1. frekwensi nafas

2. frekwensi denyut nadi

Bila terjadi peningkatan detak nafas > 5 kali/menit dan denyut nadi > 25 kali /menit dalam pemantauan setiap 4 jam berturutan, kurangi volume pemberian formula. Setelah normal kembali, ulangi menaikkan volume seperti di atas.

3. Timbang anak setiap pagi sebelum diberi makan

Setelah fase transisi dilampaui, anak diberi:

* Formula WHO 100/pengganti/Modisco 1 dengan jumlah tidak terbatas dan sering.
* Energi : 150-220 Kkal/kg bb/hari
* Protein 4-6 gram/kg bb/hari
* Bila anak masih mendapat ASI, teruskan, tetapi juga beri formula WHO 100/Pengganti/Modisco 1, karena energi dan protein ASI tidak akan mencukupi untuk tumbuh-kejar.

Setelah fase rehabilitasi (minggu ke 3-7) anak diberi :

* Formula WHO-F 135/pengganti/Modisco 1½ dengan jumlah tidak terbatas dan sering
* Energi : 150-220 kkal/kgbb/hari
* Protein 4-6 g/kgbb/hari

* Bila anak masih mendapat ASI, teruskan ASI, ditambah dengan makanan Formula ( lampiran 2 ) karena energi dan protein ASI tidak akan mencukupi untuk tumbuh-kejar.
* Secara perlahan diperkenalkan makanan keluarga

Pemantauan fase rehabilitasi

Kemajuan dinilai berdasarkan kecepatan pertambahan badan :

* Timbang anak setiap pagi sebelum diberi makan.
* Setiap minggu kenaikan bb dihitung.

o Baik bila kenaikan bb ³ 50 g/Kg bb/minggu.
o Kurang bila kenaikan bb < 50 g/Kg bb/minggu, perlu re-evaluasi menyeluruh.

TAHAPAN PEMBERIAN DIET
FASE STABILISASI : FORMULA WHO 75 ATAU PENGGANTI
FASE TRANSISI : FORMULA WHO 75 Ô FORMULA WHO 100 ATAU PENGGANTI
FASE REHABILITASI : FORMULA WHO 135 (ATAU PENGGANTI)

¯

MAKANAN KELUARGA

8. Lakukan penanggulangan kekurangan zat gizi mikro

Semua pasien KEP berat/Gizi buruk, mengalami kurang vitamin dan mineral. Walaupun anemia biasa terjadi, jangan tergesa-gesa memberikan preparat besi (Fe). Tunggu sampai anak mau makan dan berat badannya mulai naik (biasanya pada minggu ke 2). Pemberian besi pada masa stabilisasi dapat memperburuk keadaan infeksinya.

Berikan setiap hari :

o Tambahan multivitamin lain

o Bila berat badan mulai naik berikan zat besi dalam bentuk tablet besi folat atau sirup besi dengan dosis sebagai berikut :

Dosis Pemberian Tablet Besi Folat dan Sirup Besi

UMUR

DAN

BERAT BADAN

TABLET BESI/FOLAT

Sulfas ferosus 200 mg + 0,25 mg Asam Folat
o Berikan 3 kali sehari

SIRUP BESI

Sulfas ferosus 150 ml
o Berikan 3 kali sehari
6 sampai 12 bulan

(7 - < 10 Kg)
¼ tablet 2,5 ml (1/2 sendok teh)
12 bulan sampai 5 tahun ½ tablet 5 ml (1 sendok teh)

o Bila anak diduga menderita kecacingan berikan Pirantel Pamoat dengan dosis tunggal sebagai berikut :

UMUR ATAU BERAT BADAN PIRANTEL PAMOAT (125mg/tablet)

(DOSIS TUNGGAL)
4 bulan sampai 9 bulan (6-<8 Kg) ½ tablet
9 bulan sampai 1 tahun (8-<10 Kg) ¾ tablet
1 tahun sampai 3 tahun (10-<14 Kg) 1 tablet
3 Tahun sampai 5 tahun (14-<19 Kg) 1 ½ tablet

o Vitamin A oral berikan 1 kali dengan dosis

Umur Kapsul Vitamin A Kapsul Vitamin A
200.000 IU 100.000 IU
6 bln sampai 12 bln - 1 kapsul
12 bln sampai 5 Thn 1 kapsul -

Dosis tambahan disesuaikan dengan baku pedoman pemberian kapsul Vitamin A

9. Berikan stimulasi sensorik dan dukungan emosional

Pada KEP berat/gizi buruk terjadi keterlambatan perkembangan mental dan perilaku, karenanya berikan :

o Kasih sayang
o Ciptakan lingkungan yang menyenangkan
o Lakukan terapi bermain terstruktur selama 15 – 30 menit/hari
o Rencanakan aktifitas fisik segera setelah sembuh
o Tingkatkan keterlibatan ibu (memberi makan, memandikan, bermain dsb)

10.Persiapan untuk tindak lanjut di rumah

Bila berat badan anak sudah berada di garis warna kuning anak dapat dirawat di rumah dan dipantau oleh tenaga kesehatan puskesmas atau bidan di desa.

Pola pemberian makan yang baik dan stimulasi harus tetap dilanjutkan dirumah setelah pasien dipulangkan dan ikuti pemberian makanan seperti pada lampiran 5, dan aktifitas bermain.

Nasehatkan kepada orang tua untuk :

o Melakukan kunjungan ulang setiap minggu, periksa secara teratur di Puskesmas
o Pelayanan di PPG (lihat bagian pelayanan PPG) untuk memperoleh PMT-Pemulihan selama 90 hari. Ikuti nasehat pemberian makanan (lihat lampiran 5) dan berat badan anak selalu ditimbang setiap bulan secara teratur di posyandu/puskesmas.
o pemberian makan yang sering dengan kandungan energi dan nutrien yang padat
o penerapan terapi bermain dengan kelompok bermain atau Posyandu
o Pemberian suntikan imunisasi sesuai jadwal

- Anjurkan pemberian kapsul vitamin A dosis tinggi (200.000 SI atau 100.000 SI ) sesuai umur anak setiap Bulan Februari dan Agustus.
BAB IV

TATA LAKSANA DIET

PADA KEP BERAT/GIZI BURUK

A. Tingkat Rumah Tangga

1. Ibu memberikan aneka ragam makanan dalam porsi kecil dan sering kepada anak sesuai dengan kebutuhan ( lihat lampiran 5)

2. Teruskan pemberian ASI sampai anak berusia 2 tahun

B. Tingkat Posyandu /PPG

1. Anjurkan ibu memberikan makanan kepada anak di rumah sesuai usia anak, jenis makanan yang diberikan mengikuti anjuran makanan (lampiran 5)

2. Selain butir 1, maka dalam rangka pemulihan kesehatan anak, perlu mendapat makanan tambahan pemulihan (PMT-P) dengan komposisi gizi mencukupi minimal 1/3 dari kebutuhan 1 hari, yaitu :

Energi 350 – 400 kalori

Protein 10 - 15 g

3. Bentuk makanan PMT-P

Makanan yang diberikan berupa :

1. Kudapan (makanan kecil) yang dibuat dari bahan makanan setempat/lokal.
2. bahan makanan mentah berupa tepung beras,atau tepung lainnya, tepung susu, gula minyak, kacang-kacangan, sayuran, telur dan lauk pauk lainnya
3. Contoh paket bahan makanan tambahan pemulihan (PMT-P) yang dibawa pulang

Contoh bahan makanan yang dibawa pulang :

Alternative Kebutuhan Paket Bahan Makanan/Anak/Hari
I Beras 60 g Telur 1 butir atau kacang-kacangan 25 g gula 15 g
II Beras 70 g Ikan 30 g -
III Ubi/singkong 150 g Kacang-kacangan 40 g gula 20 g
V Tepung ubi 40 g Kacang-kacangan 40 g gula 20 g

4. Lama PMT-P

pemberian makanan tambahan pemulihan (PMT-P) diberikan setiap hari kepada anak selama 3 bulan (90 hari)

5. Cara penyelenggaraan

1. Makanan kudapan diberikan setiap hari di Pusat Pemulihan Gizi (PPG) atau
2. Seminggu sekali kader melakukan demonstrasi pembuatan makanan pendamping ASI/makanan anak, dan membagikan makanan tersebut kepada anak balita KEP, selanjutnya kader membagikan paket bahan makanan mentah untuk kebutuhan 6 hari.

3. Tingkat Puskesmas

Tata laksana diet pada balita KEP berat/gizi buruk ditujukan untuk memberikan makanan tinggi energi, tinggi protein, dan cukup vitamin mineral secara bertahap, guna mencapai status gizi optimal. Ada 4 (empat) kegiatan penting dalam tata laksana diet, yaitu : pemberian diet, pemantauan, dan evaluasi, penyuluhan gizi, serta tindak lanjut.

9. Pemberian diet balita KEP berat/gizi buruk harus memenuhi syarat sebagai berikut :

1. Melalui 3 fase yaitu : fase stabilisasi, fase transisi, dan fase rehabilitasi
2. Kebutuhan energi mulai 100-200 kal/Kgbb/hari
3. Kebutuhan protein mulai 1-6 g/Kgbb/hari
4. Pemberian suplementasi vitamin dan mineral khusus, bila tidak tersedia diberikan bahan makanan sumber mineral tertentu (lihat hal 12)
5. Jumlah cairan 130-200 ml/kgbb/hari, bila ada edema dikurangi menjadi 100 ml/Kg bb/hari
6. Jumlah pemberian peroral atau lewat pipa nasogastrik
7. Porsi makanan kecil dan frekwensi makan sering
8. Makanan fase stabilisasi harus hipoosmolar, rendah laktosa, dan rendah serat
9. Terus memberikan ASI
10. Makanan padat diberikan pada fase rehabilitasi dan berdasarkan berat badan, yaitu : bb < 7 kg diberikan kembali makanan bayi dan bb > 7 Kg dapat langsung diberikan makanan anak secara bertahap

Tabel 1 :

KEBUTUHAN GIZI MENURUT FASE PEMBERIAN MAKAN

ZAT GIZI FASE
STABILISASI TRANSISI
REHABILITASI
Energi 100 Kkal/kgbb/hr 150 Kkal/kgbb/hr 150-200 Kkal/kgbb/hr
Protein 1-1,5 g/kgbb/hr 2-3 g/kgbb/hr 4-6 g/kgbb/hr
Vitamin A Lihat langkah 8 Lihat langkah 8 Lihat langkah 8
Asam Folat Idem Idem Idem
Zink Idem Idem Idem
Cuprum Idem Idem Idem
Fe Idem Idem Idem
Cairan 130 ml/Kgbb/hr atau

100 ml/kgbb/hr bila ada edema
150 ml/Kgbb/hr 150-200 ml/Kgbb/hr

Tabel 2

JADWAL, JENIS, DAN JUMLAH MAKANAN YANG DIBERIKAN

FASE

WAKTU PEMBERIAN

JENIS MAKANAN

FREKWENSI JUMLAH CAIRAN (ml) SETIAP MINUM MENURUT BB ANAK
4 Kg 6 Kg 8 Kg 10 Kg
Stabilisasi Hari 1-2

Hari 3-4

Hari 5-7
F75/modifikasi/Modisco ½

F75/modifikasi/Modisco½

F75/Modifikasi/Modisco ½
12 x ( dg ASI )

12 x ( tanpa ASI)

8 x ( dg ASI)

8 x (tanpa ASI)

6 x (dg ASI)

6 x (Tanpa ASI)
45

45

65

65

90

90
65

65

100

100

130

130
-

90

-

130

-

175
-

110

-

160

-

220
Transisi Minggu 2-3
F100/modifi

kasi/Modisco I

Atau II
4 x ( dg ASI )

6 x ( tanpa ASI)
130

90
195

130
-

175
-

220
Rehabilita

Si

BB < 7 Kg
Minggu 3-6

F135/modifi

kasi/Modisco III, ditambah

Makanan lumat/makan

lembik

sari buah
3 x ( dg/tanpa ASI )

3 x 1 porsi

1 x
90

-

100
100

-

100
150

-

100
175

-

100
BB >7 Kg Makanan lunak/makan

An biasa

Buah
3 x 1 porsi

1 –2 x 1 buah
-

-
-

-
-

-
-

-

*) 200 ml = 1 gelas

Contoh :

Kebutuhan anak dengan berat badan 6 Kg pada fase rehabilitasi diperlukan :

Energi : 1200 Kkal

400 kalori dipenuhi dari 3 kali 100 cc F 135 ditambah 800 kalori dari 3 kali makanan lumat/makanan lembik dan 1 kali 100 cc sari buah

Tabel 3

FORMULA WHO
Bahan Per 100 ml
F 75
F 100 F 135
FORMULA WHO
Susu skim bubuk g 25 85 90
Gula pasir g 100 50 65
Minyak sayur g 30 60 75
Larutan elektrolit Ml 20 20 27
Tambahan air s/d Ml 1000 1000 1000
NILAI GIZI
Energi Kalori 750 1000 1350
Protein g 9 29 33
Lactosa g 13 42 48
Potasium Mmol 36 59 63
Sodium Mmol 6 19 22
Magnesium Mmol 4.3 7.3 8
Seng Mg 20 23 30
Copper Mg 2.5 2.5 3.4
% energi protein - 5 12 10
% energi lemak - 36 53 57
Osmolality Mosm/l 413 419 508

Tabel 4

MODIFIKASI FORMULA WHO
FASE STABILISASI
TRANSISI
REHABILITASI
Bahan Makanan F75 I F75 II F75

III
M½ F100 M1 MII F135 MIII
Susu skim bubuk (g) 25 - - 100 - 100 100 - -
Susu full cream (g) - 35 - - 110 - - 25 120
Susu sapi segar (ml) - - 300 - - - - - -
Gula pasir (g) 70 70 70 50 50 50 50 75 75
Tepung beras (g) 35 35 35 - - - - 50 -
Tempe (g) - - - - - - - 150 -
Minyak sayur (g) 27 17 17 25 30 50 - 60 -
Margarine (g) - - - - - - 50 - 50
Lar. Elektrolit (ml) 20 20 20 - 20 - - 27 -
Tambahan air (L) 1 1 1 1 1 1 1 1 1

*) M : Modisco

Keterangan :

1. Fase stabilisasi diberikan Formula WHO 75 atau modifikasi.

Larutan Formula WHO 75 ini mempunyai osmolaritas tinggi sehingga kemungkinan tidak dapat diterima oleh semua anak, terutama yang mengalami diare. Dengan demikian pada kasus diare lebih baik digunakan modifikasi Formula WHO 75 yang menggunakan tepung

2. Fase transisi diberikan Formula WHO 75 sampai Formula WHO 100 atau modifikasi
3. Fase rehabilitasi diberikan secara bertahap dimulai dari pemberian Formula WHO 135 sampai makanan biasa

CARA MEMBUAT

1. Larutan Formula WHO75

Campurkan susu skim, gula, minyak sayur, dan larutan elektrolit, diencerkan dengan air hangat sedikit demi sedikit sambil diaduk sampai homogen dan volume menjadi 1000 ml. Larutan ini bisa langsung diminum

Larutan modifikasi :

Campurkan susu skim/full cream/susu segar, gula, tepung, minyak. Tambahkan air sehingga mencapai 1 L (liter) dan didihkan hingga 5-7 menit.

2. Larutan Formula WHO 100 dan modifikasi Formula WHO 100

Cara seperti membuat larutan Formula WHO 75

Larutan modifikasi :

Tempe dikukus hingga matang kemudian dihaluskan dengan ulekan (blender, dengan ditambah air). Selanjutnya tempe yang sudah halus disaring dengan air secukupnya. Tambahkan susu, gula, tepung beras, minyak, dan larutan elektrolit. Tambahkan air sampai 1000 ml, masak hingga mendidih selama 5-7 menit.

3. Larutan elektrolit

Bahan untuk membuat 2500 ml larutan elektrolit mineral, terdiri atas :

KCL 224 g

Tripotassium Citrat 81 g

MgCL2.6H2O 76 g

Zn asetat 2H2O 8,2 g

Cu SO4.5H2O 1,4 g

Air sampai larutan menjadi 2500 ml (2,5 L)

Ambil 20 ml larutan elektrolit, untuk membuat 1000 ml Formula WHO 75, Formula WHO 100, atau Formula WHO 135. Bila bahan-bahan tersebut tidak tersedia, 1000 mg Kalium yang terkandung dalam 20 ml larutan elektrolit tersebut bisa didapat dari 2 gr KCL atau sumber buah-buahan antara lain sari buah tomat (400 cc)/jeruk (500cc)/pisang (250g)/alpukat (175g)/melon (400g).

2. EVALUASI DAN PEMANTAUAN PEMBERIAN DIET

1. Timbang berat badan sekali seminggu, bila tidak naik kaji penyebabnya (asupan gizi tidak adequat, defisiensi zat gizi, infeksi, masalah psikologis).
2. Bila asupan zat gizi kurang, modifikasi diet sesuai selera.
3. Bila ada gangguan saluran cerna (diare, kembung,muntah) menunjukkan bahwa formula tidak sesuai dengan kondisi anak, maka gunakan formula rendah atau bebas lactosa dan hipoosmolar, misal: susu rendah laktosa, formula tempe yang ditambah tepung-tepungan.
4. Kejadian hipoglikemia : beri minum air gula atau makan setiap 2 jam

III.PENYULUHAN GIZI DI PUSKESMAS

1. Menggunakan leaflet khusus yang berisi jumlah, jenis, dan frekwensi pemberian bahan makanan
2. Selalu memberikan contoh menu (lampiran 6)
3. Mempromosikan ASI bila anak kurang dari 2 tahun
4. Memperhatikan riwayat gizi (lampiran 3 dan 4)
5. Mempertimbangkan sosial ekonomi keluarga
6. Memberikan demonstrasi dan praktek memasak makanan balita untuk ibu

IV.TINDAK LANJUT

1. Merencanakan kunjungan rumah
2. Merencanakan pemberdayaan keluarga

Stroke, Ischemic

2009-02-15T16:27:00.000-08:00

Introduction
Background

Stroke is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Also previously called cerebrovascular accident (CVA) or stroke syndrome, stroke is a nonspecific term encompassing a heterogeneous group of pathophysiologic causes, including thrombosis, embolism, and hemorrhage.

Strokes currently are broadly classified as either hemorrhagic or ischemic. Acute ischemic stroke refers to stroke caused by thrombosis or embolism and accounts for 85% of all strokes.

Emergency physicians (EPs) play a central role in the initial evaluation and management of patients with acute stroke. In 1992, a National Institute of Neurologic Disorders and Stroke (NINDS) t-PA Pilot Trial succeeded at enrolling patients within 90 minutes, which led to the NINDS requirement that investigators from emergency medicine be involved in the larger randomized trial. The NINDS recombinant tissue-type plasminogen activator (rt-PA) stroke study group first reported that the early administration of rt-PA benefited carefully selected patients with acute ischemic stroke.1

The trial had a positive outcome leading to the current goal of t-PA administration within a 3-hour window for a patient deemed likely to benefit from thrombolytic intervention. The collaboration between emergency physicians and neurologists was visionary and enabled the early enrollment of patients, which was an integral component of the positive results. Encouraged by this breakthrough study and the subsequent approval of t-PA for use in acute ischemic stroke by the US Food and Drug Administration, many medical professionals now newly consider acute ischemic stroke to be a medical emergency—one that may be amenable to treatment.

Building on the success of the NINDS trial and other studies, the European Cooperative Acute Stroke Study III (ECASS III) examined the use of thrombolytic therapy between 3 and 4.5 hours after the onset of symptoms. Thrombolytic therapy was again found to be efficacious in improving neurologic outcomes, suggesting a wider time window for the administration of thrombolytics.2

Since EPs play a central role in the initial evaluation and treatment of patients with acute ischemic stroke, our understanding of its pathophysiology, clinical presentation, and ED evaluation is essential. The EP also must be completely familiar with the entire therapeutic armamentarium currently available to treat acute ischemic stroke, which includes supportive care, treatment of neurologic complications, antiplatelet therapy, glycemic control, blood pressure control, prevention of hyperthermia, and thrombolytic therapy.

In recent years, significant advances have also been made in stroke prevention, supportive care, and rehabilitation. With emerging evidence that the brief counsel of emergency physicians may impact primary and secondary prevention of disease processes, the emergency medicine specialty is also challenged to be vigilant in utilizing "teachable moments" or "brief negotiated interviews" to impact patient education, awareness, and compliance with established preventative treatments. Overall, when the direct costs (care and treatment) and the indirect costs (lost productivity) of strokes are considered together, the cost to US society is $43.3 billion per year.3
Pathophysiology

On the macroscopic level, ischemic stroke most often is caused by extracranial embolism or intracranial thrombosis, but it may also be caused by decreased cerebral blood flow. On the cellular level, any process that disrupts blood flow to a portion of the brain unleashes an ischemic cascade, leading to the death of neurons and cerebral infarction. Understanding this chain of events is important for understanding current therapeutic approaches.

Embolism

Emboli may arise from the heart, the extracranial arteries or, rarely, the right-sided circulation (paradoxical emboli) with subsequent passage through a patent foramen ovale. The sources of cardiogenic emboli include valvular thrombi (eg, in mitral stenosis, endocarditis, prosthetic valve), mural thrombi (eg, in myocardial infarction [MI], atrial fibrillation [AF], dilated cardiomyopathy, severe congestive heart failure [CHF]), and atrial myxoma. MI is associated with a 2-3% incidence of embolic stroke, of which 85% occur in the first month after MI.4

Thrombosis

Thrombotic stroke can be divided into large vessel, including the carotid artery system, or small vessel comprising the intracerebral arteries, including the branches of the Circle of Willis and the posterior circulation. The most common sites of thrombotic occlusion are cerebral artery branch points, especially in the distribution of the internal carotid artery. Arterial stenosis can cause turbulent blood flow, which can increase risk for thrombus formation, atherosclerosis (ie, ulcerated plaques), and platelet adherence; all cause the formation of blood clots that either embolize or occlude the artery.

Less common causes of thrombosis include polycythemia, sickle cell anemia, protein C deficiency, fibromuscular dysplasia of the cerebral arteries, and prolonged vasoconstriction from migraine headache disorders. Any process that causes dissection of the cerebral arteries also can cause thrombotic stroke (eg, trauma, thoracic aortic dissection, arteritis). Occasionally, hypoperfusion distal to a stenotic or occluded artery or hypoperfusion of a vulnerable watershed region between two cerebral arterial territories can cause ischemic stroke.

Flow disturbances

Stroke symptoms can result from inadequate cerebral blood flow due to decreased blood pressure (and specifically decreased cerebral perfusion pressure) or due to hematologic hyperviscosity due to sickle cell disease or other hematologic illnesses such as multiple myeloma and polycythemia vera. In these instances, cerebral injury may occur in the presence of damage to other organ systems.

Ischemic cascade

Within seconds to minutes of the loss of perfusion to a portion of the brain, an ischemic cascade is unleashed that, if left unchecked, causes a central area of irreversible infarction surrounded by an area of potentially reversible ischemic penumbra.

On the cellular level, the ischemic neuron becomes depolarized as ATP is depleted and membrane ion-transport systems fail. The resulting influx of calcium leads to the release of a number of neurotransmitters, including large quantities of glutamate, which, in turn, activates N -methyl-D-aspartate (NMDA) and other excitatory receptors on other neurons. These neurons then become depolarized, causing further calcium influx, further glutamate release, and local amplification of the initial ischemic insult. This massive calcium influx also activates various degradative enzymes, leading to the destruction of the cell membrane and other essential neuronal structures.5

Free radicals, arachidonic acid, and nitric oxide are generated by this process, which leads to further neuronal damage. Within hours to days after a stroke, specific genes are activated, leading to the formation of cytokines and other factors that, in turn, cause further inflammation and microcirculatory compromise.5 Ultimately, the ischemic penumbra is consumed by these progressive insults, coalescing with the infracted core, often within hours of the onset of the stroke.

The central goal of therapy in acute ischemic stroke is to preserve the area of oligemia in the ischemic penumbra. The area of oligemia can be preserved by limiting the severity of ischemic injury (ie, neuronal protection) or by reducing the duration of ischemia (ie, restoring blood flow to the compromised area).

The ischemic cascade offers many points at which such interventions could be attempted. Multiple strategies and interventions for blocking this cascade are currently under investigation. The timing of the restoration of cerebral blood flow appears to be a critical factor. Time also may prove to be a key factor in neuronal protection. Although still being studied, neuroprotective agents, which block the earliest stages of the ischemic cascade (eg, glutamate receptor antagonists, calcium channel blockers), are expected to be effective only in the proximal phases of presentation.
Frequency
United States

Incidence for first-time stroke is more than 700,000 per year, of which 20% of these patients will die within the first year after stroke. At current trends, this number is projected to jump to 1 million per year by the year 2050.6
International

Global incidence of stroke is unknown.
Mortality/Morbidity

Stroke is the third leading cause of death and the leading cause of disability in the United States.7

* Cerebrovascular disease was the second leading cause of death worldwide in 1990, killing more than 4.3 million people.8
* Cerebrovascular disease was also the fifth leading cause of lost productivity, as measured by disability-adjusted life years (DALYs). DALYs include years of productivity lost to either death or varying degrees of disability. In 1990, cerebrovascular disease caused 38.5 million DALYs throughout the world.9

Sex

Men are at higher risk for stroke than women. Additionally, women seem to respond better than men to interventions such as rt-PA.
Age

Although stroke often is considered a disease of elderly persons, one third of strokes occur in persons younger than 65 years.6
Clinical
History

* Stroke should be considered in any patient presenting with an acute neurologic deficit (focal or global) or altered level of consciousness.
* No historical feature distinguishes ischemic from hemorrhagic stroke, although nausea, vomiting, headache, and change in level of consciousness are more common in hemorrhagic strokes.
* Common symptoms of stroke include abrupt onset of hemiparesis, monoparesis, or quadriparesis; monocular or binocular visual loss; visual field deficits; diplopia; dysarthria; ataxia; vertigo; aphasia; or sudden decrease in the level of consciousness.
* Although such symptoms can occur alone, they are more likely to occur in combination.
* Establishing the time of onset of these symptoms is of paramount importance when considering patients for possible thrombolytic therapy. An essential question is, "When was the patient last seen normal?" It is advisable for emergency clinicians to rapidly enlist the assistance of family members or relatives to establish time of onset and to identify other pertinent components of the patient's history of presentation. The median time from symptom onset to ED presentation ranges from 4-24 hours in the United States.10
* Multiple factors contribute to delays in seeking care for symptoms of stroke.
o Many strokes occur while patients are sleeping (also known as "wake-up" stroke) and are not discovered until the patient wakes.
o Stroke can leave some patients too incapacitated to call for help.
o Occasionally, a stroke goes unrecognized by the patient or their caregivers.6, 11
* Stroke mimics commonly confound the clinical diagnosis of stroke. One study reported that 19% of patients diagnosed with acute ischemic stroke by neurologists before cranial CT scanning actually had noncerebrovascular causes for their symptoms. The most frequent stroke mimics include seizure (17%); systemic infection (17%); brain tumor (15%); toxic-metabolic cause, such as hyponatremia (13%); and positional vertigo (6%). Miscellaneous disorders mimicking stroke include syncope, trauma, subdural hematoma, herpes encephalitis, transient global amnesia, dementia, demyelinating disease, myasthenia gravis, parkinsonism, hypertensive encephalopathy, and conversion disorders. A critical masquerading metabolic derangement not to be missed by providers is hypoglycemia.12, 13

Physical

* The goals of the physical examination include detecting extracranial causes of stroke symptoms, distinguishing stroke from stroke mimics, determining and documenting for future comparison the degree of deficit, and localizing the lesion.
* The physical examination always includes a careful head and neck examination for signs of trauma, infection, and meningeal irritation.
* A careful search for the cardiovascular causes of stroke requires examination of the ocular fundi (retinopathy, emboli, hemorrhage), heart (irregular rhythm, murmur, gallop), and peripheral vasculature (palpation of carotid, radial, and femoral pulses, auscultation for carotid bruit).
* Patients with a decreased level of consciousness should be assessed to ensure that they are able to protect their airway.
* Neurologic examination
o With the availability of thrombolytic therapy for acute ischemic stroke in selected patients, the EP must be able to perform a brief but accurate neurologic examination on patients with suspected stroke syndromes.
o The goals of the neurologic examination include (1) confirming the presence of a stroke syndrome (to be defined further by cranial CT scanning), (2) distinguishing stroke from stroke mimics, and (3) establishing a neurologic baseline should the patient's condition improve or deteriorate.
o Essential components of the neurologic examination include evaluation of mental status and the level of consciousness, cranial nerves, motor function, sensory function, cerebellar function, gait, and deep tendon reflexes.
o The skull and spine also should be examined, and signs of meningismus should be sought.
o Central facial weakness from a stroke should be differentiated from the peripheral weakness of Bell palsy. With peripheral lesions (Bell palsy), the patient is unable to lift the eyebrows or wrinkle the forehead.
o The 4 principal neuroanatomic stroke syndromes are caused by disruption of their respective cerebrovascular distributions. Correlating the patient's neurologic deficits with the expected site of arterial compromise may assist in confirming the diagnosis of stroke and interpreting the subsequent cranial CT scan.
o Middle cerebral artery (MCA) occlusion commonly produces contralateral hemiparesis, contralateral hypesthesia, ipsilateral hemianopsia, and gaze preference toward the side of the lesion. Agnosia is common, and receptive or expressive aphasia may result if the lesion occurs in the dominant hemisphere. Neglect, inattention, and extinction of double simultaneous stimulation may occur in nondominant hemisphere lesions. Since the MCA supplies the upper extremity motor strip, weakness of the arm and face is usually worse than that of the lower limb.
o Anterior cerebral artery occlusions primarily affect frontal lobe function and can result in dis-inhibition and speech perseveration, producing primitive reflexes (eg, grasping, sucking reflexes), altered mental status, impaired judgment, contralateral weakness (greater in legs than arms), contralateral cortical sensory deficits gait apraxia, and urinary incontinence.
o Posterior cerebral artery occlusions affect vision and thought, producing contralateral homonymous hemianopsia, cortical blindness, visual agnosia, altered mental status, and impaired memory.
o Vertebrobasilar artery occlusions are notoriously difficult to detect because they cause a wide variety of cranial nerve, cerebellar, and brainstem deficits. These include vertigo, nystagmus, diplopia, visual field deficits, dysphagia, dysarthria, facial hypesthesia, syncope, and ataxia. A hallmark of posterior circulation stroke is that there are crossed findings: ipsilateral cranial nerve deficits and contralateral motor deficits. This is contrasted to anterior stroke, which produces only unilateral findings.
o Lacunar strokes result from occlusion of the small, perforating arteries of the deep subcortical areas of the brain. The infarcts are generally from 2-20 mm in diameter. The most common lacunar syndromes include pure motor, pure sensory, and ataxic hemiparetic strokes. Lacunar infarcts are often associated with partial or full occlusion of the parent feeding artery. Lacunar strokes account for 13-20% of all cerebral infarctions. Lacunar infarcts commonly occur in patients with small vessel disease, such as diabetes and hypertension. By virtue of their small size and well-defined subcortical location, lacunar infarcts do not lead to impairments in cognition, memory, speech, or level of consciousness.
o Stroke scales
+ The National Institutes of Health Stroke Scale (NIHSS) is a rapid and reproducible tool for quantifying neurologic deficits in stroke patients and is useful for following the patient's early course. It is advisable to use this scale because it provides a means of quantitatively following a patient's course (ie, rapidly improving symptoms, or, escalation of symptoms secondary to either a bleed or cerebral edema).
+ The NIHSS is a 42-point scale with minor strokes usually being considered to have a score less than 5. A NIHSS score greater than 10 correlates with an 80% likelihood of visual flow deficits on angiography. Discretion must be also be used in assessing the magnitude of the clinical deficit; for instance, if a patient's only deficit is being mute, then the NIHSS score will be 3. Additionally, the scale does not measure some deficits associated with posterior circulation strokes (ie, vertigo, ataxia).14

Causes

* Risk factors
o Briefly assessing the risk factors for stroke may provide clues as to its cause and reinforce the clinical gestalt that clinicians may have in uncertain situations. Risk factors for ischemic stroke include advanced age (the risk doubles every decade), hypertension, smoking, heart disease (coronary artery disease, left ventricular hypertrophy, chronic atrial fibrillation), and hypercholesterolemia. Hyperhomocysteinemia has also been identified as an independent risk factor for all forms of stroke.15
o Diseases associated with increased blood viscosity and the use of oral contraceptives place patients at higher risk for ischemic stroke.
o Previous cerebrovascular disease is a risk factor for ischemic stroke.
* Transient ischemic attack
o Transient ischemic attack (TIA) has come to be known as a neurologic deficit that resolves within 24 hours. Roughly 80% resolve within 60 minutes. Tissue-based definitions are being proposed with magnetic resonance imaging.15
o TIA can result from any of the aforementioned mechanisms of stroke. Data suggest that roughly 10% of patients with TIA suffer stroke within 90 days and half of these patients suffer stroke within 2 days.15, 16

TBC HIV

2009-02-15T16:24:00.000-08:00

Tuberculosis and HIV have been closely linked since the emergence of AIDS. HIV infection has contributed to a significant increase in the worldwide incidence of tuberculosis.(1,2) By producing a progressive decline in cell-mediated immunity, HIV alters the pathogenesis of tuberculosis, greatly increasing the risk of developing disease in coinfected individuals and leading to more frequent extrapulmonary involvement and atypical radiographic manifestations. Although HIV-related tuberculosis is both treatable and preventable, incidence rates continue to climb in developing nations where HIV infection and tuberculosis are endemic and resources are limited. Worldwide, tuberculosis is the most common opportunistic infection affecting HIV-seropositive individuals,(1) and it is the most common cause of death in patients with AIDS.(3) This chapter will review the epidemiology, pathogenesis, and management of tuberculosis in the setting of HIV infection.
transparent image
Epidemiology of HIV-Related Tuberculosis
transparent image

The World Health Organization (WHO) estimates that one-third of the world's population is infected with Mycobacterium tuberculosis, resulting in an estimated 8 million new cases of tuberculosis and nearly 2 million deaths each year.(4) Approximately 10 million people are estimated to be coinfected with M tuberculosis and HIV, and over 90% of these dually infected individuals reside in developing nations. In some areas of sub-Saharan Africa, the rates of coinfection exceed 1,000 per 100,000 population (Figure 1).(5) Worldwide, tuberculosis is the most common cause of death among patients with AIDS, killing 1 of every 3 patients.(3)

After decades of steady decline, tuberculosis cases increased in 1986 in the United States.(6) Between 1985 and 1990, tuberculosis cases increased by 20%, resulting in 28,040 excess cases of tuberculosis. The U.S. Centers for Disease Control and Prevention (CDC) estimates that AIDS-related tuberculosis accounted for a minimum of 30% of these excess cases.(7) Fortunately, tuberculosis cases have been declining in the United States since 1992.(8) Between 1992 and 1999, tuberculosis cases decreased by nearly 34%. HIV-related cases have also declined. From 1993 to 1998, the proportion of HIV-related cases has decreased from 29% to 20% in the 25- to 44-year-old age group.(8)

The prevalence of HIV infection among tuberculosis cases varies greatly from state to state. Unfortunately, in 1999, only half the states had HIV test results in >=75% of tuberculosis cases.(8) For these jurisdictions, mean HIV seroprevalence rate was 17.9%, with a range of 0-44.1%. The District of Columbia, Florida, and New York City each had HIV seroprevalence rates >40% among their tuberculosis cases, whereas Texas, South Carolina, Utah, and Georgia had rates >=30%.

The decline in HIV-related tuberculosis in the United States and other industrialized countries has paralleled an overall decline in tuberculosis cases. Whether or not the use of effective antiretroviral therapy (ART) has hastened this decline is not clear. Two cohort studies have described the frequency of tuberculosis during the current era of treatment.(9,10) In the Frankfurt AIDS cohort study of 1,000 HIV-infected homosexual men with CD4 T-lymphocyte counts <200 cells/mm3, the overall incidence of AIDS-defining conditions decreased by >70% between 1992 and 1996.(9) However, the rate of tuberculosis, although low, remained stable over the study period. In contrast, the EuroSIDA cohort study of 7,000 HIV-infected patients reported dramatic declines in the rate of tuberculosis and disseminated Mycobacterium avium complex (MAC) from the period before 1993 to the period after 1997, coinciding with the introduction of potent ART.(10) Further studies are needed to assess the impact of antiretroviral therapy on the rates of tuberculosis in different populations.
transparent image
Drug-Resistant Tuberculosis
transparent image

Paralleling the increase in tuberculosis cases in the United States was an increase in the number of cases of drug-resistant tuberculosis. The frequency of multidrug-resistant tuberculosis (MDRTB) in the United States increased from 0.4% in the early 1980s to 3.5% in 1991, with most of the MDRTB cases residing in New York.(11) The CDC investigated at least eight MDRTB outbreaks that occurred in New York, New Jersey, and Miami, and reported that approximately 90% of the cases were HIV seropositive.(12) In New York, previously treated patients, those with HIV infection, and injection drug users were all at increased risk of having drug-resistant tuberculosis.(13) A study of HIV-infected and -uninfected individuals with tuberculosis in eight U.S. centers participating in a community-based clinical trials group found a 20.4% prevalence of tuberculosis resistant to one or more drugs, with 5.6% of the isolates resistant to both isoniazid (INH) and rifampin.(14) In multiple logistic regression analyses, HIV infection was shown to be a risk factor for having drug-resistant tuberculosis, independent of geographic location, history of prior therapy, age, or race.

Recent studies have found that HIV-seropositive patients are more likely to develop acquired drug resistance (ADR) than seronegative cases.(15-18) In a case-control study involving 16 cases of ADR in San Francisco between 1990 and 1994, AIDS, nonadherence to the tuberculosis treatment regimen, and gastrointestinal symptoms were each independently associated with the acquisition of drug resistance.(17) During the study period one of every 16 AIDS patients with tuberculosis, and either gastrointestinal symptoms or nonadherence, developed ADR. Of note, most of the patients developed mono-rifampin-resistant tuberculosis, which is an unusual form of ADR. It is not clear why acquired mono-rifampin-resistant tuberculosis would be more likely to arise in HIV-1-seropositive persons, although malabsorption of antituberculosis drugs has been postulated as a causative factor.(17)
transparent image
Impact of HIV Infection on the Pathogenesis of Tuberculosis
transparent image

Tuberculosis can develop through progression of recently acquired infection (primary disease), reactivation of latent infection, or exogenous reinfection. Recent data suggest that in urban areas within the United States, recent transmission accounts for a larger proportion of cases than was realized previously.(19,20) Molecular genotyping studies in San Francisco and New York reported that 30-40% of new cases were due to recent infection with rapid progression to disease. In both studies, HIV infection or AIDS was an independent risk factor for recent acquisition of infection and rapid progression to disease.

Infection with M tuberculosis can occur when an individual exposed to an infectious case of tuberculosis inhales particles (<5 µm in size) containing the tubercle bacilli.(21) If the bacilli reach the pulmonary alveoli, they may be ingested by alveolar macrophages, the first line of defense against M tuberculosis. Surviving tubercle bacilli multiply within the macrophage and eventually undergo hematogenous spread to other areas of the body. Although defects in macrophage function have been demonstrated in HIV-infected patients, there is no conclusive evidence that HIV-seropositive persons are more likely to acquire tuberculous infection than HIV-seronegative individuals, given the same degree of exposure.(22)

Once infection does occur, however, the risk of rapid progression is much greater among persons with HIV infection, because HIV impairs the host's ability to contain new tuberculous infection. Immunocompetent individuals infected with M tuberculosis have approximately a 10% lifetime risk of developing tuberculosis,(23) with half of the risk occurring in the first 1-2 years after infection. In contrast, a San Francisco study reported rapid spread of tuberculosis during an outbreak in a residential care facility for HIV-seropositive substance abusers.(24) Among the 30 residents who were exposed to possible infection, 11 (37%) developed tuberculosis within 106 days, and at least one person developed tuberculosis within 4 weeks of exposure, demonstrating the rapidity with which tuberculosis can spread within an HIV-infected population.

Several cohort studies have demonstrated a high incidence of active tuberculosis among HIV-infected individuals with positive tuberculin skin test results (Table 1).(25-30) However, the rates of active tuberculosis have varied considerably depending on the population and region studied. For example, among cohorts of HIV-infected injection drug users with positive skin tests, the annual rate of tuberculosis has varied from 4.5 to 10.4 cases per 100 person-years. These variations in the incidence rate of tuberculosis are likely due to differences in the prevalence of actual tuberculous infection (as opposed to false-positive skin tests) among the cohorts, differences in the severity of immunosuppression, and the amount of ongoing transmission that was occurring in the cohorts.

Infection with M tuberculosis in an immunocompetent person is thought to confer significant protective immunity against exogenous reinfection.(23) However, reinfection has been reported in HIV-seronegative(31,32) and -seropositive individuals,(33-37) although its incidence is not known. DNA fingerprinting on paired isolates of M tuberculosis from 17 patients who had repeatedly positive cultures at a single hospital in New York City found four patients to have acquired a new, drug-resistant strain of M tuberculosis through exogenous reinfection, probably as a result of nosocomial transmission.(33)

Because of the increased virulence in immunocompetent hosts of M tuberculosis compared with other opportunistic pathogens (eg, Pneumocystis jiroveci), tuberculosis can occur early in the course of HIV infection. In several studies of HIV-infected patients with pulmonary tuberculosis, the median CD4 T-cell count was >300 cells/mm3.(38) However, in patients with primarily extrapulmonary involvement or disseminated disease, the CD4 T-cell count may be much lower. For example, two studies in African patients with disseminated disease found the median CD4 T-cell count to be <80 cells/mm3.(38) A prospective study in the United States,(25) found the median CD4 T-cell count to be 144 cells/mm3 (range 2-543) in HIV-infected patients with all forms of tuberculosis. Although tuberculosis can be a relatively early manifestation of HIV-1 infection, it is important to note that the risk of developing tuberculosis, and of disseminated infection, increases as the CD4 T-cell count decreases.
transparent image
Impact of Tuberculosis on the Natural History of HIV Infection
transparent image

Although the immune response to M tuberculosis is important in controlling disease, immune activation may also be associated with increased HIV viral load and accelerated progression of HIV infection. A retrospective cohort study in the United States found that although only one patient in the group died of tuberculosis, HIV-infected patients with tuberculosis do not survive as long as HIV-infected controls without tuberculosis, even after controlling for baseline CD4 T-cell count. When tuberculin-positive HIV-infected patients were given INH therapy in Haiti, they were less likely to develop AIDS and less likely to die than patients given placebo.(39) Thus, it is likely that tuberculosis acts to accelerate the clinical course of HIV infection.

Although increased viral replication is thought to play a role, the mechanisms by which tuberculosis accelerates progression of HIV disease are not known with certainty. High levels of tumor necrosis factor (TNF)-alpha, which are known to increase HIV replication in T-cell clones,(40) have been demonstrated in both HIV-1-seropositive and -seronegative tuberculosis cases.(41). Moreover, investigators have shown that M tuberculosis or purified protein derivative can also increase viral replication in infected T lymphocytes and monocytes.(42-44) A recent study demonstrated a 5- to 160-fold increase in viral replication during the acute phase of untreated tuberculosis.(40) The clinical significance of this increase in viral load is uncertain.
transparent image
Clinical Presentation and Diagnosis
transparent image
transparent image
Clinical Presentation of Tuberculosis
transparent image

The clinical presentation of pulmonary tuberculosis can vary widely in both immunocompetent and immunocompromised hosts. In general, the presentation in the HIV-infected patient is similar to that seen in HIV-uninfected patients, although the signs and symptoms (such as fevers, weight loss, and malaise) may be attributed to HIV itself and the possibility of tuberculosis overlooked. Symptoms are usually present for weeks to months, and the acute onset of fever and cough is more suggestive of a nonmycobacterial pulmonary process. If there is no response to antimicrobial therapy, however, the possibility of tuberculosis should be considered. In HIV-infected patients, clinical manifestations of pulmonary tuberculosis reflect different levels of immunosuppression. Earlier in the course of HIV disease, tuberculosis is more likely to present as classical reactivation-type disease, whereas patients with advanced immunosuppression are more likely to present with findings consistent with primary tuberculosis (see Radiographic Findings, below).

The prevalence of extrapulmonary tuberculosis is increased in HIV-infected patients. Low CD4 T-cell counts are associated with an increased frequency of extrapulmonary tuberculosis, positive mycobacterial blood cultures, and atypical chest radiographic findings, reflecting an inability of the impaired immune response to contain infection.(45) Patients with extrapulmonary tuberculosis may present with signs and symptoms specific to the involved site, such as lymphadenopathy, headache, meningismus, pyuria, abscess formation, back pain, or abdominal pain. These findings in HIV-infected patients can present a diagnostic challenge. Whenever possible, diagnostic specimens should be examined for acid-fast bacilli (AFB) and cultured for mycobacteria.
transparent image
Radiographic Findings
transparent image

The chest radiograph is the cornerstone of diagnosis for pulmonary tuberculosis. Upper lobe infiltrates and cavities are the typical findings in reactivation tuberculosis, whereas intrathoracic lymphadenopathy and lower lobe disease are seen in primary tuberculosis. In HIV-infected persons with higher CD4 T-cell counts (eg, >200 cells/mm3) the radiographic pattern tends to be one of reactivation disease with upper lobe infiltrates with or without cavities.(46) In HIV-infected persons who have a greater degree of immunosuppression (eg, CD4 T-cell count <200 cells/mm3), a pattern of primary disease with intrathoracic lymphadenopathy and lower lobe infiltrates is seen (Figure 2 and Figure 3). As chest radiographs may appear normal in 7-14% of cases, a high index of suspicion must be maintained in evaluating an HIV-infected patient with symptoms suggestive of tuberculosis.(47,48) In the authors' experience, the finding of low-density lymph nodes with peripheral enhancement on a contrast-enhanced chest computed tomography (CT) scan is highly predictive of tuberculosis.
transparent image
Bacteriologic Examinations
transparent image

All patients suspected of having pulmonary tuberculosis should have 3 sputum specimens obtained on 3 consecutive days, and these specimens should be examined for AFB and cultured for mycobacteria. AFB identified on smear are not diagnostic of tuberculosis, as the acid-fast stain detects mycobacteria other than M tuberculosis, including M avium-intracellulare complex or M kansasii. However, until identification is confirmed, empiric therapy for tuberculosis should be initiated if the sputum smear is positive for AFB. The rate of AFB smear positivity has varied from 31% to 89% in HIV-positive patients.(49) In general, the rate of smear positivity correlates with the extent of radiographic disease. For example, patients with cavitary lesions due to active tuberculosis will almost always have positive smears, whereas a negative smear in a patient with minimal disease on chest radiograph would not be unusual, and would not rule out active tuberculosis. However, in HIV-infected patients positive smears may be seen with relatively little radiographic involvement.

When expectorated sputum specimens are AFB smear-negative, further evaluation may be indicated. Bronchoscopy with bronchoalveolar lavage and transbronchial biopsy may be useful in the evaluation of an abnormal chest radiograph when sputum smears are negative. In this setting, a rapid diagnosis of presumptive tuberculosis, based on histology and AFB smear of specimens obtained by bronchoscopy, can be made in 30-40% of individuals, which is similar to the yield of bronchoscopy in HIV-negative cases with smear-negative pulmonary tuberculosis.(50).

Positive cultures for M tuberculosis provide a definitive diagnosis of tuberculosis. Approximately 15% of reported tuberculosis cases are culture negative, but these data are not available for HIV-infected cases. However, at San Francisco General Hospital, culture-negative tuberculosis in HIV-infected patients is seldom observed. (This perceived increase in sensitivity may be due in part to the increased use of diagnostic bronchoscopy in HIV-positive cases of suspected tuberculosis.) Unfortunately, culture results may not be available for 2-6 weeks, creating a need for more rapid diagnostic techniques. Nucleic acid amplification (NAA) tests detect nucleic acid sequences unique to organisms in the M tuberculosis complex, allowing for a rapid diagnosis. Two NAA tests, the Amplified Mycobacterium Tuberculosis Direct Test (MTD; Gen-Probe) and the Amplicor Mycobacterium Tuberculosis Test (Amplicor; Roche) have been approved by the U.S. Food and Drug Administration (FDA) for use in respiratory specimens in patients who have not previously been treated for tuberculosis. The MTD test is approved for use in smear-positive or smear-negative samples, whereas Amplicor is only approved for use with smear-positive samples. A suggested algorithm and guide for interpreting NAA test results has recently been published,(51) but local tuberculosis control agencies may have their own guidelines for the use of these newer tests. A negative NAA test does not rule out the diagnosis of active tuberculosis, and antituberculous therapy and further diagnostic workup are needed if sufficient clinical suspicion for tuberculosis exists. The predictive value of NAA testing will vary depending on the sensitivity and specificity of the test in the local laboratory, as well as on the prevalence of M tuberculosis and other mycobacteria. Moreover, NAA testing does not provide information on drug resistance. NAA tests are an important addition to our armamentarium of diagnostic tools, but they do not replace AFB smear, culture, or, more importantly, clinical judgment.
transparent image
Treatment of HIV-Related Tuberculosis
transparent image

HIV-seropositive patients with tuberculosis respond well to antituberculosis therapy, as long as the regimen contains INH and a rifamycin. The treatment of HIV-related tuberculosis requires close monitoring because of frequent drug toxicities, possible drug-drug interactions, and paradoxical reactions.

There have been six prospective studies, four randomized and two observational in nature, of 6-month treatment regimens for active tuberculosis (Table 2).(52-57) Because these studies differed in design, patient population, eligibility criteria, site of disease, frequency of dosing, dose administration, and outcome definitions, it is difficult to provide meaningful cross-study comparisons. It is important to note, however, that all of the studies reported a good, early clinical response to therapy, and the time in which M tuberculosis sputum cultures converted from positive to negative and treatment failure rates were similar to those in patients without HIV infection.

The recurrence rates vary between studies. Although most studies reported recurrence rates of 5% or less among HIV-infected cases, two studies reported rates close to 10%. In Kinshasa, Zaire, patients with tuberculosis were treated with INH, rifampin, pyrazinamide, and ethambutol daily for 2 months, followed by INH and rifampin twice weekly for 4 months.(52) Only one-half of the doses in the continuation phase were directly observed. The HIV-seropositive cases were then randomized to receive an additional 6 months of placebo or twice-weekly INH and rifampin. There was no statistically significant difference in the recurrence rates between the HIV-seropositive (9%) and -seronegative subjects (5.3%). HIV-seropositive cases who received the extended therapy had a recurrence rate of 1.9% compared with 9% in the placebo group (p < .01). Despite a lower recurrence rate in the HIV seropositive subjects who received extended therapy, there was no difference in survival compared with those who did not receive the extended treatment. The reasons for the higher recurrence rate in the HIV seropositive patients is unknown, but may have been because of nonadherence in the continuation phase or exogenous reinfection.

The Tuberculosis Trials Consortium, sponsored by the CDC, conducted a randomized trial of rifapentine versus rifampin in the continuation phase of therapy.(57) Adults who had completed a 2-month induction phase of INH, rifampin, pyrazinamide, and ethambutol were randomly assigned to receive 900 mg INH and 600 mg rifampin twice weekly, or 900 mg INH and 600 mg rifapentine once weekly. Seventy-one HIV-infected patients were enrolled, of whom 61 completed therapy and were assessed for relapse. Five of 30 (17%) patients in the once-weekly INH/rifapentine arm relapsed, compared with three of 31 (10%) patients in the twice-weekly INH/rifampin arm. Four of the five relapses in the once-weekly group had monoresistance to rifampin, compared with none in the standard treatment arm. Enrollment of HIV-infected patients with tuberculosis was halted in the study because of these findings. The authors concluded that HIV-infected patients with tuberculosis should not be treated with a once-weekly INH and rifapentine regimen.

In another Tuberculosis Trials Consortium study, an intermittent rifabutin-based regimen was evaluated. This was a single-arm trial of twice-weekly rifabutin-based therapy in HIV-infected persons. Five patients who failed treatment or relapsed developed acquired rifamycin resistance. All five had low CD4 counts (<60 cells/mm3). Four received twice-weekly therapy in the first 2 months of treatment, and all five received twice-weekly therapy in the continuation phase. Based on these findings, for HIV-infected persons with CD4 counts <100 cells/mm3, daily therapy is indicated during the first 2 months, followed by either daily therapy or three doses per week during the continuation phase.(58)
transparent image
Rifampin- vs. Rifabutin-Based Regimens
transparent image

Rifabutin is another rifamycin that is highly active against M tuberculosis. Compared with rifampin, rifabutin shows less induction of hepatic microsomal metabolism. Limited data suggests that rifabutin- and rifampin-based regimens are equally efficacious. A randomized clinical trial in Argentina, Brazil, and Thailand compared rifabutin (at two dosages) with rifampin.(59) A total of 520 HIV-negative patients were enrolled and randomly assigned to receive either rifampin (n = 175), rifabutin 150 mg (n = 174), or rifabutin 300 mg (n = 171). The mean time to culture conversion was similar between groups. There was one relapse in the rifampin group and two in each of the rifabutin groups. A randomized trial in South Africa compared rifabutin to rifampin in a standard four-drug regimen administered in directly observed therapy (DOT).(60) In the continuation phase, the medications were given twice weekly. The mean time to sputum conversion was 14.1 weeks with rifampin versus 14.3 weeks with rifabutin. The difference in relapse rates between the two regimens (3.8% in the rifampin group and 5.1% in the rifabutin group) was not statistically significant.

In the only such trial done in HIV-infected patients--a single-blind, randomized study of 50 HIV-infected patients in Uganda--compared a fully supervised regimen of rifampin versus rifabutin together with INH, ethambutol, and pyrazinamide.(61) Time to sputum conversion was similar between groups when controlling for baseline characteristics.
transparent image
Safety and Tolerability
transparent image

The frequency of adverse drug reactions has varied considerably between studies. In two different studies from San Francisco, 18-26% of HIV-seropositive patients with tuberculosis underwent a change in therapy because of adverse drug reactions.(62,63) Rifampin was the drug most commonly implicated, producing an adverse reaction in 12% of the patients. In Zaire, 11% of the seropositive cases developed a rash, but treatment was not interrupted.(52) Paresthesia was common and developed in 21% of cases, pointing out the need for coadministration of pyridoxine (vitamin B6) when INH is used in HIV-1-seropositive individuals. Other investigators have reported low rates of drug reactions.(53,54) Differences between studies in the reported frequency of adverse drug reactions may reflect different patient populations, different degrees of immunosuppression among the patients, and different thresholds of providers to change therapy.

Antituberculosis drug-induced hepatotoxicity is common among HIV-infected patients with and without hepatitis C infection. One study found the relative risk of developing drug-induced hepatotoxicity in patients with hepatitis C or HIV infection to be fivefold and fourfold, respectively.(64) The relative risk of developing drug-induced hepatitis in patients with both hepatitis C and HIV infection was increased 14-fold. Frequent monitoring of liver function tests during tuberculosis treatment may be indicated in patients with hepatitis C.

Thiacetazone, which is used in many developing countries for the treatment of tuberculosis, has been reported to cause frequent and significant skin reactions in HIV-seropositive patients being treated for tuberculosis.(65,66) In one study, up to 20% of the HIV-seropositive patients on thiacetazone developed cutaneous rashes, compared with 1% of the seronegative cases; the case-fatality rate was 14% in the HIV-seropositive persons suffering these reactions.(66) The risk of cutaneous reactions in a randomized trial of thiacetazone- and rifampin-containing regimens was nearly 10 times higher in the seropositive cases compared to the seronegative cases.(65) These reports prompted the WHO to abandon thiacetazone in the treatment of HIV-related tuberculosis.(2)
transparent image
Current American Thoracic Society/CDC Treatment Recommendations
transparent image

Recommendations for the treatment of tuberculosis in HIV-infected patients are identical to those for HIV-uninfected cases, with two exceptions: a) once-weekly INH-rifapentine in the continuation phase should not be used; and b) twice-weekly INH-rifampin or rifabutin should not be used for patients with CD4 lymphocyte counts <100 cells/mm3 (Table 3).(67) A 6-month (26-week) regimen consisting of INH, rifampin, and pyrazinamide given for 2 months, followed by INH and rifampin for 4 months is the preferred treatment for drug-susceptible organisms (Table 4). Ethambutol or streptomycin should be added to the above regimen until drug susceptibility results are available. In HIV-infected cases, the 6-month regimen should be considered the minimum duration of treatment. It is very important to assess the clinical and bacteriologic response in the setting of HIV-1 infection. Patients with cavitation on initial chest radiograph and positive culture at completion of 2 months of therapy should receive a 7-month (31-week) continuation phase. Antituberculosis therapy that contains INH should be supplemented with pyridoxine (vitamin B6) at 25-50 mg per day to prevent the development of peripheral neuropathy.

The most important factor in the treatment of HIV-related tuberculosis is adherence to the treatment regimen. DOT should be considered in all HIV-infected patients. At least one study reported a decreased mortality in HIV-infected patients who received DOT versus self-administered therapy.(68)
transparent image
Drug-Drug Interactions
transparent image

Successful therapy for tuberculosis requires that HIV-infected individuals take antituberculosis drugs for a minimum of 6 months, in addition to potentially large numbers of other medications. Certain antituberculosis drugs may interact adversely with medications commonly used by HIV-infected individuals. Understanding these drug-drug interactions can prevent drug toxicity and possible treatment failures.

The rifamycin derivatives (ie, rifampin, rifabutin, and rifapentine) can induce the hepatic cytochrome P450 enzyme system, resulting in increased metabolism and serum levels of certain drugs.(69) Medications that are known to be affected include fluconazole, ketoconazole, methadone, oral contraceptives, phenytoin, protease inhibitors (PIs), and nonnucleoside reverse transcriptase inhibitors (NNRTIs) (69,70). Coadministration of rifampin with ketoconazole or fluconazole decreases the area under the curve (AUC) of the antifungal by approximately 80% and 20%, respectively.(69) Therefore, ketoconazole and rifampin should not be given together. Rifampin and fluconazole can be used together, but the fluconazole dose may need to be increased.

Combination ART is commonly used for the treatment of HIV infection. These agents are divided into nucleoside reverse transcriptase inhibitors (NRTIs), NNRTIs, and PIs. The rifamycin derivatives accelerate the metabolism of the PIs and NNRTIs resulting in subtherapeutic levels and the potential development of viral resistance to these important agents(70). Of the available rifamycins, rifampin is the most potent inducer of the P450 enzymes and thus produces significant reductions in the serum concentrations of the PIs and NNRTIs. Rifabutin, which is a less potent inducer of the P450 enzymes, can be substituted for rifampin in the treatment regimen. However, because the PIs and NNRTIs affect the metabolism of rifabutin, resulting in altered serum levels and the possibility of drug toxicity, adjustments in rifabutin dosage are often necessary. The CDC recently published pharmacokinetic data regarding the rifamycins and the PIs and NNRTIs (Table 5 and Table 6).(71) These data can be used to design treatment regimens for HIV and tuberculosis.

Patients can take the standard rifampin-based treatment regimen if they will not be taking PIs or NNRTIs. Previous guidelines specifically stated that rifampin was contraindicated for patients who were taking any PI or NNRTI.(72) However, new data indicate that rifampin can be used for the treatment of tuberculosis with certain combinations of antiretroviral agents (Table 5 and Table 6).(71) (As discussed above, for patients who are taking PIs or NNRTIs, rifabutin may be substituted for rifampin with proper dose adjustments to rifabutin and the antiretrovirals.)
transparent image
Paradoxical Reaction
transparent image

Some patients may experience a temporary exacerbation of symptoms, signs, or radiographic manifestations of tuberculosis after beginning antituberculosis treatment. This worsening has been referred to as a "paradoxical reaction" and has been noted to occur in HIV-infected patients with active tuberculosis. These reactions often develop after immune reconstitution has occurred in the setting of simultaneous administration of both antiretroviral and antituberculosis medications. A prospective study in Florida found that 36% of HIV patients who were taking antiretroviral agents, compared with 7% who were not, developed a paradoxical worsening of their clinical and/or radiographic condition.(73) The diagnosis of a paradoxical reaction should be made only after a thorough evaluation to exclude other etiologies, such as tuberculosis treatment failure.

Symptomatic therapy is sufficient for patients with a paradoxical reaction in whom the symptoms are not severe or life-threatening. For patients whose reactions are associated with severe or life-threatening conditions (eg, uncontrollable fever, airway compromise from enlarging lymph nodes, enlarging serosal fluid collections, sepsis syndrome), management may include the use of corticosteroids. Some experts recommend that prednisone (or equivalent corticosteroid) be started at a dose of 1 mg/kg and reduced after 1-2 weeks based on the resolution of symptoms.
transparent image
Initiation of Antiretroviral Therapy in the Coinfected Patient
transparent image

It is not unusual for the diagnosis of tuberculosis and HIV to be made simultaneously. In this setting, treatment of tuberculosis should be initiated immediately. Whether or when to initiate ART is a more difficult decision. Some experts argue that delaying treatment of HIV infection for 2 months, observing for any adverse effects from the tuberculosis medicines, and potentially decreasing the risk of a paradoxical reaction is a reasonable approach. On the other hand, effective ART can have a significant impact on HIV-related morbidity and mortality. A recent study from Narita and colleagues described the successful use of rifabutin in combination with an antiretroviral regimen containing PIs.(74) All 25 patients became culture negative for M tuberculosis by 2 months of treatment, and no relapses were reported during a median follow-up of 13 months. Moreover, the HIV viral load decreased significantly with 20 of 25 patients achieving viral loads of <500 copies/mL. Thus, it appears that tuberculosis and HIV can be treated concurrently using a rifabutin-based regimen.

In patients already receiving ART, the regimen should be continued, and modifications to either the tuberculosis regimen or to the antiretroviral regimen can be made as indicated. Whether it is best to start ART as soon as possible or wait until antituberculosis treatment is well established is not clear at present, so the decision should be made on a case-by-case basis, taking into account factors related to both adherence (such as motivation and stability of living situation) and potential for complications (such as clinically active hepatitis C). Involvement of the patient in the decision of whether and when to start ART is crucial.

It is important to be aware of the potential problems that can occur when antituberculosis medications and antiretroviral agents are administered concurrently. Gastrointestinal complaints and rash are not uncommon with antituberculosis medications and these can be quite common with certain antiretroviral medications. A flulike illness has been described with rifampin, which could be confused with an abacavir hypersensitivity reaction. Peripheral neuropathy is an adverse effect of INH as well as stavudine and didanosine. Elevated liver function tests can occur with INH, rifampin, pyrazinamide, and most of the NRTIs, NNRTIs, and PIs.

It can be challenging to determine which medication is the offending agent. In the setting of tuberculosis, this usually involves holding all medications and restarting sequentially to determine which medication caused the problem. Although this approach works quite well with tuberculosis medications, in the case of HIV infection, sequential addition of antiretroviral drugs is not advisable because of the risk of developing antiretroviral resistance. When an adverse reaction occurs with antiretroviral medications, the agent most likely to be responsible is usually deduced based on known adverse-effect profiles and clinical judgement.
transparent image
Diagnosis and Treatment of Latent Tuberculosis Infection
transparent image
transparent image
Diagnosis of Latent Tuberculosis Infection
transparent image

Screening for latent tuberculosis infection (LTBI) is an essential step in controlling the spread of tuberculosis. Screening for LTBI is recommended in persons at risk for recent infection and in those groups with increased risk of progression to active disease once infected, including HIV-infected persons. The tuberculin skin test (Mantoux method) is currently the only method available for identifying LTBI. Routine annual tuberculin skin testing is recommended in HIV-infected individuals. A reaction of >=5 mm induration is considered positive for HIV-infected patients and persons with other forms of severe immunosuppression, persons who are close contacts of infectious cases, and persons with abnormal chest radiographs consistent with tuberculosis.(75). Use of the 5-mm cutoff is supported by a prospective study in the United States demonstrating that the risk of tuberculosis was significantly higher in HIV-infected persons with tuberculin skin test reactions >=5 mm of induration than in those who have a reaction <5 mm.(25)

It is important to keep in mind that a negative tuberculin skin test does not exclude infection or active disease. Testing with tuberculin purified protein derivative is dependent on the presence of an intact cell-mediated immune response. In the setting of HIV infection, reduced cell-mediated immunity can lead to decreased delayed-type hypersensitivity (DTH) responsiveness, resulting in false-negative skin tests. In a multicenter study in the United States, the prevalence of a positive tuberculin skin test (>=5 mm) was shown to decrease with decreasing CD4 T-cell counts.(76) Persons who are at risk for tuberculous infection (eg, injection drug users, individuals who are institutionalized or from high-prevalence regions) should have a chest radiograph performed even if the tuberculin skin test is negative, particularly if their CD4 T-cell count is low. Annual chest radiographs should be considered in this high-risk group.

Application of multiple skin test antigens (eg, Candida, mumps, tetanus toxoid, etc.), referred to as anergy testing, has been used to assess cell-mediated immune function and to distinguish true-negative from false-negative tuberculin skin test results. In 1991, the CDC recommended that anergy testing be performed in conjunction with tuberculin skin testing in HIV-infected persons based on the premise that anergic HIV-infected individuals at high risk for tuberculosis infection would benefit from treatment with INH.(77) In 1997, the CDC revised its recommendations and no longer recommends anergy testing while screening for M tuberculosis infection in HIV-infected persons.(78) The revised recommendation is based on the following points. First, there are no standardized guidelines for performing anergy skin testing. The appropriate number of control antigens to administer or the appropriate cut-off for interpreting a test as positive is not known. Second, the response to skin testing with control antigens as well as with tuberculin can vary over time. Several studies have demonstrated that HIV-1-seropositive individuals can regain DTH responsiveness with time.(29,72,79) In a multicenter study, Chin and colleagues(79) reported that 31% of anergic HIV-1-seropositive patients responded to DTH testing 1 year later. The only factor associated with regaining DTH responsiveness was the CD4 T-cell count: the higher the CD4 count, the more likely the individual was to regain DTH responsiveness. Finally, treatment of LTBI in anergic HIV-infected persons has not been demonstrated to be beneficial.(80,81)

In some individuals with tuberculous infection, DTH responsiveness may decrease with time. A second tuberculin skin test, applied weeks to months after the first, can "boost" the DTH response resulting in a positive skin test reaction. Such responses are considered true evidence of tuberculous infection. In a multicenter study in the United States, only 2.7% of HIV-1-seropositive patients "boosted" the tuberculin reaction with a second tuberculin skin test, despite relatively high demographic risk of tuberculous infection.(82) However, a study in Uganda found that 17 (29%) of 58 HIV-1-infected subjects responded to a second tuberculin skin test.(83) Because most groups in the United States have a relatively low prevalence of tuberculosis, two-step tuberculin skin testing is not recommended routinely.
transparent image
Treatment of Latent Tuberculosis Infection
transparent image

HIV-infected individuals with LTBI have an extraordinarily high rate of progression to active tuberculosis compared to HIV-uninfected persons. Fortunately, treatment of LTBI is very effective in preventing persons infected with M tuberculosis from developing active disease. Annual screening of all HIV-infected persons for LTBI, and treatment of those coinfected with M tuberculosis, is therefore recommended. Treatment regimens for LTBI are not adequate for the treatment of active tuberculosis, and may select for drug-resistant strains if inadvertently used in the setting of active disease. Therefore, after a positive skin test, active tuberculosis must be ruled out before providing treatment for latent infection.

There have been two placebo-controlled trials with INH in tuberculin-positive, HIV-infected patients (Table 7).(39,81) Investigators in Haiti reported the results of the first randomized, placebo-controlled study of INH given for 6 months.(39) Treatment with INH significantly reduced the rate of tuberculosis compared with placebo (10.0 vs. 1.7 per 100 person-years) in tuberculin-positive individuals. A placebo-controlled study in Uganda compared four treatment arms: placebo for 6 months, INH for 6 months, INH and rifampin for 3 months, and INH, rifampin, and pyrazinamide for 3 months.(81) As shown in Table 7, all of the treatment arms significantly reduced the rate of tuberculosis compared with placebo.

Three prospective, randomized trials have compared 2-3 months of the dual-drug regimen rifampin plus pyrazinamide to 6-12 months of INH.(84-86) The most recent of these trials demonstrated that 2 months of daily rifampin and pyrazinamide was as effective as 12 months of daily INH in HIV-infected persons.(86) Studies have also found intermittent dosing of INH,(84,85) or pyrazinamide plus rifampin,(84,85) to be effective, but intermittent dosing has not been directly compared with daily regimens.
transparent image
Current American Thoracic Society/CDC Recommendations
transparent image

Until recently, a 6- or 12-month course of INH was the recommended regimen for treatment of LTBI in HIV-seronegative and -seropositive persons, respectively. The current guidelines from the American Thoracic Society and CDC offer three options for the treatment of LTBI in HIV-infected persons based on the studies described above (Table 8).(75) The first option is to give INH daily or twice weekly for 9 months instead of the previous recommendation of 12 months. This new recommendation is generalized from data in HIV-uninfected persons that 12 months of INH is more efficacious than 6 months of therapy in preventing active tuberculosis but that minimal benefit is gained by extending treatment from 9 to 12 months.(87) The second option for treatment of LTBI is rifampin plus pyrazinamide administered daily for 2 months. However, since the above guidelines were published, 21 cases of liver injury, including five deaths, have been reported in HIV-uninfected persons receiving a 2-month regimen of rifampin and pyrazinamide. The American Thoracic Society and CDC have prepared new recommendations given these unexpected findings. For HIV-uninfected persons, 9 months of INH is the preferred regimen. Four months of daily rifampin would be the next alternative (discussed below). The 2-month rifampin-pyrazinamide regimen should be used with caution, only in patients who can be closely monitored and for whom the likelihood of completing a longer treatment course is unlikely. Even though trials of 2-3 months of rifampin and pyrazinamide in HIV-infected persons did not show increased risk of severe hepatitis, it may be advisable to use 9 months of INH until more is known about the frequency of, and risk factors for, toxicity in HIV-infected persons.(88) The third regimen for treatment of LTBI is rifampin daily for 4 months. Rifampin alone for 3 months was shown to be more efficacious than placebo in HIV-negative persons with silicosis.(89) However, because the rate of active TB was still high at 10%, the recommendation is to extend the duration of therapy to 4 months for both HIV-infected and -uninfected persons who cannot tolerate INH or pyrazinamide.

Although there are no studies of rifabutin-containing regimens in the treatment of LTBI, rifabutin appears to be equal in efficacy to rifampin in the treatment of tuberculosis. Therefore, rifabutin can be substituted for rifampin in cases where rifampin is contraindicated. An INH-containing regimen should be supplemented with pyridoxine (25-50 mg/day) to prevent the development of peripheral neuropathy.

HIV-infected individuals who are close contacts of persons with infectious tuberculosis should receive treatment for LTBI regardless of the results of the tuberculin skin test, as long as active tuberculosis has been ruled out.(90,75) In addition, because exogenous reinfection has been demonstrated in patients with AIDS, treatment should be given even if a prior course of therapy for tuberculosis or LTBI has been completed.(33) Contacts of known cases of INH-resistant tuberculosis should be treated with rifampin (600 mg/day) instead of INH. Close contacts to MDRTB cases should be treated with at least two drugs to which the source isolate is susceptible.

Morbus Hansen (Lepra)

2009-02-15T16:23:00.001-08:00

Introduction

Background

Leprosy is a chronic infection caused by the acid-fast, rod-shaped bacillus Mycobacterium leprae. Leprosy can be considered 2 connected diseases that primarily affect superficial tissues, especially the skin and peripheral nerves. Initially, a mycobacterial infection causes a wide array of cellular immune responses. These immunologic events then elicit the second part of the disease, a peripheral neuropathy with potentially long-term consequences.

The social and psychological effects of leprosy, as well as its highly visible debilities and sequelae, have resulted in a historical stigma associated with leprosy (see Image 1). To minimize the prejudice against those with leprosy, the condition is also known as Hansen disease, named after G.A. Hansen, who is credited with the 1873 discovery of M leprae. This mycobacterium grows extremely slowly and has not been successfully cultured in vitro.

In the 1990s, the World Health Organization (WHO) launched a campaign to eliminate leprosy as a public health problem by 2000. Elimination, as defined by the WHO, was defined as a reduction of patients with leprosy requiring multidrug therapy to fewer than 1 per 10,000 population. This goal was achieved in terms of global prevalence by 2002, but 15 of the 122 countries where leprosy was endemic in 1985 still have prevalence rates of greater than 1 per 10,000 population.¹

Although multidrug regimens have been used globally to cure nearly 14 million patients with leprosy since 1985, the number of new leprosy cases remained relatively unchanged from 1980 to 2000, ranging from 500,000-700,000 worldwide per year.² Access and delivery of antibiotics continues to be a problem in the most endemic nations. With the precise transmission mechanism of leprosy still unknown and a lack of an effective vaccine, leprosy will probably continue to pose an ongoing public health problem in the coming decades.

Pathophysiology

Leprosy can manifest in different forms, depending on the host response to the organism.

Individuals who have a vigorous cellular immune response to M leprae have the tuberculoid form of the disease that usually involves the skin and peripheral nerves. The number of skin lesions is limited, and they tend to be dry and hypoesthetic. Nerve involvement is usually asymmetric. This form of the disease is also referred to as paucibacillary leprosy because of the low number of bacteria in the skin lesions (ie, <5>

Individuals with minimal cellular immune response have the lepromatous form of the disease, which is characterized by extensive skin involvement. Skin lesions are often described as infiltrated nodules and plaques, and nerve involvement tends to be symmetric in distribution. The organism grows best at 27-30°C; therefore, skin lesions tend to develop in the cooler areas of the body, with sparing of the groin, axilla, and scalp. This form of the disease is also referred to as multibacillary leprosy because of the large number of bacteria found in the lesions (ie, >6 lesions, with possible visualization of bacilli on smear). Results of skin tests with antigen from killed organisms are nonreactive.

Patients may also present with features of both categories; however, over time, they usually evolve to one or the other (indeterminate or borderline leprosy). Interestingly, most individuals who are exposed to leprosy never develop the disease.

Classification of leprosy: Leprosy has 2 classification schemas: the 5-category Ridley-Jopling system and the simpler and more commonly used WHO standard.

Ridley-Jopling: Depending on the host response to the organism, leprosy can manifest clinically along a spectrum bounded by the tuberculoid and lepromatous forms of the disease. Most patients fall into the intermediate classifications, which include borderline tuberculoid leprosy, midborderline leprosy, and borderline lepromatous leprosy. The classification of the disease typically changes as it evolves during its progression or management. The Ridley-Jopling system is used globally and forms the basis of clinical studies of leprosy. It may also be more useful in guiding treatment regimens and assessing risk of acute complications. Physical findings in each subtype are presented in the Clinical section.
WHO system: The WHO recommends classifying leprosy according to the number of lesions and the presence of bacilli on a skin smear. This method is useful in countries where biopsy analysis in unavailable.
- Paucibacillary leprosy is characterized by 5 or fewer lesions with absence of organisms on smear. Paucibacillary leprosy generally includes the tuberculoid and borderline lepromatous categories from the Ridley-Jopling system.
- Multibacillary leprosy is marked by 6 or more lesions with possible visualization of bacilli on smear. Lepromatous leprosy, borderline lepromatous leprosy, and midborderline leprosy on the Ridley-Jopling scale are included in the multibacillary leprosy category.

Frequency

United States

In the United States, an average of 150 cases are diagnosed each year. In 2004, 69 new cases of leprosy were detected and 131 total persons were reported to have the disease, according to the WHO. Most cases of leprosy in the United States are found in immigrants, although endemic foci exist in parts of Louisiana, Florida, and Texas along the Gulf of Mexico; in Mexican and Asian California populations; and in Spanish Americans in New York City. Around 85% of these detected leprosy cases involve patients who have lived in foreign countries, primarily Asia, Africa, and Latin America.³

International

According to WHO figures, the global registered prevalence of leprosy at the start of 2005 was 286,063 cases. Global annual detection rates have declined from 2001 to 2004, when 763,262 and 407,791 new cases were reported, respectively. Leprosy is still deemed a public health problem in 9 countries: Angola, Brazil, Central African Republic, Democratic Republic of the Congo, India, Madagascar, Mozambique, Nepal, and the United Republic of Tanzania. These countries account for 84% of reported cases. Furthermore, more than 94% of new cases of leprosy in Latin America are reported in Brazil.¹

Mortality/Morbidity

Leprosy is rarely fatal, and the primary consequence of infection is nerve impairment and debilitating sequelae. According to one study, 33-56% of newly diagnosed patients already displayed signs of impaired nerve function.⁴ According to estimates, 3 million people who have completed multidrug therapy for leprosy have sustained disability due to nerve damage. Although both lepromatous leprosy and tuberculoid leprosy involve the skin and peripheral nerves, tuberculoid leprosy has more severe manifestations. Nerve involvement results in loss of sensory and motor function, which may lead to frequent trauma and amputation. The ulnar nerve is most commonly involved.

Damage in the following nerves is associated with characteristic impairments in leprosy:
- Ulnar and median - Clawed hand
- Posterior tibial - Plantar insensitivity and clawed toes
- Common peroneal -Foot drop
- Radial cutaneous, facial, and greater auricular nerves (may also be involved; see Image 2)
Infiltration by bacteria may lead to destruction of nasal cartilage (lepromatous leprosy), ocular involvement, and diffuse thickening of the skin. Advanced cases of leprosy involve the loss of eyebrows and lashes, but these deformities are less common today.
Worldwide, leprosy is considered the most common cause of crippling of the hand, which is caused by ulnar nerve involvement.⁵ Peroneal nerve involvement can lead to foot drop, posterior tibial nerve involvement, and clawed toes.

Race

Leprosy was once endemic worldwide, and no racial predilection is known. In the late 1800s, the incidence of leprosy in northern Europe and North America dropped dramatically, and the disease is now reported primarily in tropical areas.

Sex

Leprosy is generally more common in males than in females, with a male-to-female ratio of 1.5:1. In some areas in Africa, the prevalence of leprosy among females is equal to or greater than that in males.²

Age

Leprosy can occur at any age, but, in developing countries, the age-specific incidence of leprosy peaks in children younger than 10 years, who account for 20% of leprosy cases. Leprosy is very rare in infants; however, they are at a relatively high risk of acquiring leprosy from the mother, especially in cases of lepromatous leprosy or midborderline leprosy.

Clinical

History

Symptoms
- Painless skin patch accompanied by loss of sensation but not itchiness (Loss of sensation is a feature of tuberculoid leprosy, unlike lepromatous leprosy, in which sensation is preserved; see Image 3.)
- Loss of sensation or paresthesias where the affected peripheral nerves are distributed
- Wasting and muscle weakness
- Foot drop or clawed hands (may result from neuritic pain and rapid peripheral nerve damage; see Image 4)
- Ulcerations on hands or feet (see Image 5)
- Lagophthalmos, iridocyclitis, corneal ulceration, and/or secondary cataract due to nerve damage and direct bacillary skin or eye invasion⁶
Symptoms in reactions
- Type 1 (reversal) - Sudden onset of skin redness and new lesions
- Type 2 (erythema nodosum leprosum [ENL]; see Image 10) - Many skin nodules, fever, redness of eyes, muscle pain, and joint pain
Travel: Leprosy should be considered in anyone who has lived in the tropics or who has traveled for prolonged periods to endemic areas.
Exposure: The incubation period of leprosy is long, ranging from a few months to 20-50 years. The mean incubation time is estimated to be 10 years for lepromatous leprosy and 4 years for tuberculoid leprosy. The organism's slow dividing time (once every 2 wk) contributes to the challenge of epidemiologically linking exposures to the development of disease.
Because of immunologic reasons, only around 5-10% of the population is estimated to be susceptible to infection.

Physical

The cardinal signs of leprosy include hypoesthesia, skin lesions, and peripheral neuropathy. The first physical signs of leprosy are usually cutaneous. The subtype of leprosy often determines the degree of skin involvement.

Physical examination should include the following:
- Evaluation of skin lesions
- Careful sensory and motor examination
- Palpation of peripheral nerves for pain or enlargement, with particular attention paid to the following locations:
  - Elbows - Ulnar nerve
  - Wrist - Superficial radial cutaneous and median nerves
  - Popliteal fossa - Common peroneal nerve
  - Neck - Great auricular nerve
Physical findings in specific leprosy subtypes include the following:
- Tuberculoid leprosy
  - The initial lesion is often a sharply demarcated hypopigmented macule that is ovoid, circular, or serpiginous. The lesions may be somewhat elevated with a dry scaly center and erythematous borders.
  - Common lesion sites include the buttocks, face, and extensor surfaces of limbs. The perineum, scalp, and axilla are not normally involved because of the temperature differential in these zones, as predilection is toward cooler zones.
  - As the disease progresses, lesions tend to destroy the normal skin organs such as sweat glands and hair follicles.
  - Superficial nerves that lead from the lesions tend to enlarge and are sometimes palpable. The patient may experience severe neuropathic pain. Nerve involvement can also lead to trauma and muscle atrophy.
- Lepromatous leprosy
  - This form is characterized by extensive bilaterally symmetric cutaneous involvement, which can include macules, nodules, plaques, or papules (see Image 6).
  - Unlike lesions in tuberculoid leprosy, those in lepromatous leprosy have poorly defined borders and raised and indurated centers. As in all forms of leprosy, lepromatous lesions are worst on cooler parts of the body. Common areas of involvement include the face, ears, wrists, elbows, buttocks, and knees.
  - Hoarseness, loss of eyebrows and eyelashes, and nasal collapse secondary to septa perforation may occur in advanced cases of disease. Involvement of the eye may include keratitis, glaucoma, or iridocyclitis (see Image 7).
  - The leonine facies associated with leprosy develop as the disease progresses, and the facial skin becomes thickened and corrugated.
  - Axillary and inguinal adenopathy may develop, in addition to scarring of the testes and subsequent gynecomastia and sterility.
  - Nerve involvement in lepromatous leprosy is not as severe as in tuberculoid leprosy, since nerves, although visibly thickened and highly infected, still function reasonably well in early stages of the disease.
- Borderline tuberculoid leprosy: The lesions are few or moderate and asymmetric with almost complete anesthesia. Peripheral nerves are often involved and thickened asymmetrically, and cutaneous nerves are sometimes enlarged.
- Midborderline leprosy: The number of skin lesions is moderate, and they are asymmetrical and somewhat anesthetic. Peripheral nerves may be somewhat symmetrically enlarged, but cutaneous nerves are not.
- Borderline lepromatous leprosy: Moderate to numerous slightly asymmetrical skin lesions appear with minor or no anesthesia. Peripheral nerves are often enlarged symmetrically, but cutaneous nerves are not.
- Indeterminate leprosy: Skin lesions are typically either hypopigmented or hyperpigmented macules or plaques. Patients may note that these lesions are anesthetic or paresthetic.

Causes

M leprae is the causative agent associated with leprosy, which has been recognized as an infectious disease for the last 2 millennia. M leprae was discovered as the causative agent in 1873. The acid fast, gram-positive bacillus is an obligate intracellular organism with a predilection for Schwann cells and macrophages. M leprae has not been successfully grown using artificial media.
The route of transmission has not been definitively established, although human-to-human aerosol spread of nasal secretions is thought to be the most likely mode of transmission in most cases. Leprosy is not spread by touch, since the mycobacteria are incapable of crossing intact skin. Living near people with leprosy is associated with increased transmission. Among household contacts, the relative risk for leprosy is increased 8- to 10-fold in multibacillary and 2- to 4-fold in paucibacillary forms. Animal reservoirs do exist (armadillos, certain nonhuman primates), and cases of suspected zoonotic transmission have been reported.

allergic rhinitis

2009-02-15T16:21:00.001-08:00

Allergic rhinitis is a collection of symptoms, predominantly in the nose and eyes, caused by airborne particles of dust, dander, or plant pollens in people who are allergic to these substances.

When these symptoms are caused by pollen, the allergic rhinitis is commonly called hay fever.

Hipertensi

2009-02-15T16:17:00.000-08:00

Hypertension, also referred to as high blood pressure, HTN or HPN, is a medical condition in which the blood pressure is chronically elevated. In current usage, the word "hypertension"^[1] without a qualifier normally refers to systemic, arterial hypertension.^[2]

Hypertension can be classified either essential (primary) or secondary. Essential hypertension indicates that no specific medical cause can be found to explain a patient's condition. Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another condition, such as kidney disease or tumours (pheochromocytoma and paraganglioma).

Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure. Even moderate elevation of arterial blood pressure leads to shortened life expectancy. At severely high pressures, defined as mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.^[3]

In individuals older than 50 years, hypertension is considered to be present when a person's systolic blood pressure is consistently 140 mm Hg or greater or when the diastolic blood pressure is consistently 90 mm Hg or greater. Beginning at a systolic pressure of 115 and diastolic pressure of 75 (commonly written as 115/75 mm Hg), cardiovascular disease (CVD) risk doubles for each increment of 20/10 mmHg.^[4] Prehypertension is defined as blood pressure from 121/81 mm Hg to 139/89 mm Hg. Prehypertension is not a disease category; rather, it is a designation chosen to identify individuals at high risk of developing hypertension.^[4] The Mayo Clinic specifies that blood pressure is normal if it is 120/80 or below.^[5] Patients with blood pressures over 130/80 mm Hg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment.^[4]

Resistant hypertension is defined as the failure to reduce BP to the appropriate level after taking a three-drug regimen.^[4] The American Heart Association released guidelines for treating resistant hypertension.^[6]

Causes

[edit] Essential (primary) hypertension

By definition, essential hypertension has no identifiable cause. However, several risk factors have been identified, including obesity,^[7] salt sensitivity, renin homeostasis, insulin resistance, genetics, and age.

[edit] Obesity

The risk of hypertension is 5 times higher in the obese as compared to those of normal weight and up to two-thirds of cases can be attributed to excess weight. More than 85% of cases occur in those with a Body mass index greater than 25.^[7]A definitive link between obesity and hypertension has been found using animal and clinical studies, from these it has been realised that many mechanisms are potential causes of obesity induced hypertension.These mechanisms include the activation of the sympathetic nervous system as well as the activation of the renin–angiotensin-aldosterone system.^[8]

[edit] Sodium sensitivity

Sodium is an environmental factor that has received the greatest attention. Approximately one third of the essential hypertensive population is responsive to sodium intake.^[9] This is because increasing the amount of salt in a person's bloodstream causes cells to release water (due to osmotic pressure) to equilibrate the concentration gradient between the cells and the bloodstream, thereby increasing the pressure within the blood vessel walls^{[citation needed]}. The increased Na+ stimulates ADH and thirst mechanisms, leading to a concentrated urine and the kidneys holding onto water along with the person increasing the intake of water. Also, the water movement between cells and the interstitium plays a minor role compared to this.

[edit] Role of renin

Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked with aldosterone in a negative feedback loop. The range of renin activity observed in hypertensive subjects tends to be broader than in normotensive individuals. In consequence, some hypertensive patients have been defined as having low-renin and others as having essential hypertension. Low-renin hypertension is more common in African Americans than white Americans, and may explain why African Americans tend to respond better to diuretic therapy than drugs that interfere with the Renin / angiotension system.

High Renin levels predispose to Hypertension: Increased Renin → Increased Angiotensin II → Increased Vasoconstriction, Thirst/ADH and Aldosterone → Increased Sodium Resorption in the Kidneys (DCT and CD) → Increased Blood Pressure. Some authorities claim that potassium might both prevent and treat hypertension.^[10]

[edit] Insulin resistance

Insulin is a polypeptide hormone secreted by cells in the islets of langerhans, which are contained throughout the pancreas. Its main purpose is to regulate the levels of glucose in the body antagonistically with glucagon through negative feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin. Insulin resistance and/or hyperinsulinemia have been suggested as being responsible for the increased arterial pressure in some patients with hypertension^{[citation needed]}. This feature is now widely recognized as part of syndrome X, or the metabolic syndrome.

[edit] Genetics

Hypertension is one of the most common complex disorders.The etiology of hypertension differs widely amongst individuals within a large population.^[11] More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing.One of these gene is angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number of AGT increases the blood pressure and hence this may cause hypertension.^[12] Twins have been included in studies measuring ambulatory blood pressure, from these studies it has been suggested that essential hypertension contains a large genetic influence. ^[13] Supporting data has emerged from animal studies as well as clinical studies in human populations.The majority of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each have an elevated blood pressure as one of their phenotypic expressions.However, the genetic influence upon hypertension is not fully understood at the moment. It is believed that linking hypertension-realted phenotypes with specific variations of the genome may yeild definitive evidence of heritability. ^[14]

Another view is that hypertension can be caused by mutations in single genes, inherited on a mendelian basis.^[15]

[edit] Age

Hypertension can also be age related, if this is the case it is likely to be multifactorial. One possible mechanism involves a reduction in vascular complicance due to the stiffening of the arteries. This can build up due to isolated systolic hypertension with a widened pulse pressure. A decrease in glomerular filtration rate is related to aging and this results in decreasing efficiency of sodium excretion. The developing of certain diseases such as renal microvascular disease and capillary rarefaction may relate to this decrease in efficiency of sodium excretion. There is experimental evidence that suggests that renal microvascular disease is an important mechanism for inducing slat-sensitive hypertension.^[16]

[edit] Vitamin D

It has been suggested, as a result of several studies, that vitamin D deficiency is associated with cardiovascular risk factors. It has been observered that individuals with a vitamin D deficiency have higher systolic and diastolic blood pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a “negative endocrine regulator of the renin-angiotensin system”. Hence a deficancy in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed link between hypertension and vitamin D levels in the blood plasma. ^[17]

[edit] Secondary hypertension

Secondary hypertension results from an identifiable cause. With treatment of the underlying cause, secondary hypertension can resolve without the need for anti-hypertensive medications.

[edit] Sleep apnea

Sleep apnea is a common, under-recognized cause of hypertension.^[18] It is often best treated with nocturnal nasal continuous positive airway pressure, but other approaches include the Mandibular advancement splint (MAS), UPPP, tonsilectomy, adenoidectomy, septoplasty, or weight loss.

[edit] Liquorice

Consumption of liquorice (which can be of potent strength in liquorice candy) can lead to a surge in blood pressure.^[19] People with hypertension or history of cardio-vascular disease should avoid liquorice raising their blood pressure to risky levels. Frequently, if liquorice is the cause of the high blood pressure, a low blood level of potassium will also be present.

Liquorice extracts are present in many medicines (for example cough syrups, throat lozenges and peptic ulcer treatments).

[edit] Renal hypertension

Hypertension produced by diseases of the kidney. This includes diseases such as polycystic kidney disease or chronic glomerulonephritis. Hypertension can also be produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the Renin / angiotension system.

[edit] Adrenal hypertension

Hypertension is a feature of a variety of adrenal cortical abnormalities. In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.

[edit] Cushing's syndrome

Cushing's syndrome is a condition where both adrenal glands can overproduce the hormone cortisol. Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. More than 80% of patients with Cushing's syndrome have hypertension.

In patients with pheochromocytoma increased secretion of catecholamines such as epinephrine and norepinephrine by a tumor (most often located in the adrenal medulla) causes excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).

[edit] Coarctation of the aorta

The congenital abnormality aortic coarctation can result in hypertension.

[edit] Drugs

Certain medications, especially NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension. Licorice (Glycyrrhiza glabra) inhibits the 11-hydroxysteroid hydrogenase enzyme (catalyzes the reaction of cortisol to cortison) which allows cortisol to stimulate the Mineralocorticoid receptor (MR) which will lead to effects similar to hyperaldosteronism, which itself is a cause of hypertension.^[20]

[edit] Rebound hypertension

High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications. The increases in blood pressure may result in blood pressures greater than when the medication was initiated. Depending on the severity of the increase in blood pressure, rebound hypertension may result in a hypertensive emergency. Rebound hypertension is avoided by gradually reducing the dose (also known as "dose tapering"), thereby giving the body enough time to adjust to reduction in dose.

Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine and beta-blockers.

[edit] Apparent mineralocorticoid excess syndrome

Main article: Apparent mineralocorticoid excess syndrome

autosomal recessive disorder results from mutations in gene encoding 11β-hydroxysteroid dehydrogenase which normal patient inactivates circulating cortisol to the less-active metabolite cortisone. Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension.

[edit] Glucocorticoid remediable aldosteronism

Main article: Glucocorticoid remediable aldosteronism

is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not.

[edit] Polycystic kidney disease

Main article: Polycystic kidney disease

is a cystic genetic disorder of the kidneys, PKD is characterized by the presence of multiple cysts (hence, "polycystic") in both kidneys, can also damage the liver, pancreas, and rarely, the heart and brain. It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being more common and characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts, with concurrent development of hypertension, renal insufficiency and renal pain.

[edit] Pregnancy

Main article: Hypertension of pregnancy

Although few women of childbearing age have high blood pressure, up to 10% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.

[edit] Pathophysiology

Most of the mechanisms associated with secondary hypertension are generally fully understood. However, those associated with essential (primary) hypertension are far less understood. What is known is that cardiac output is raised early in the disease course, with total peripheral resistance (TPR) normal; over time cardiac output drops to normal levels but TPR is increased. Three theories have been proposed to explain this:

Inability of the kidneys to excrete sodium, resulting in natriuretic factors such as Atrial Natriuretic Factor being secreted to promote salt excretion with the side-effect of raising total peripheral resistance.
An overactive Renin / angiotension system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension.
An overactive sympathetic nervous system, leading to increased stress responses.

It is also known that hypertension is highly heritable and polygenic (caused by more than one gene) and a few candidate genes have been postulated in the etiology of this condition.^[21]^[22]^[23]

[edit] Diagnosis

[edit] Measuring blood pressure

Main article: Blood pressure

Diagnosis of hypertension is generally on the basis of a persistently high blood pressure. Usually this requires three separate measurements at least one week apart. Exceptionally, if the elevation is extreme, or end-organ damage is present then the diagnosis may be applied and treatment commenced immediately.

Obtaining reliable blood pressure measurements relies on following several rules and understanding the many factors that influence blood pressure reading.^[24]

For instance, measurements in control of hypertension should be at least 1 hour after caffeine, 30 minutes after smoking or strenuous exercise and without any stress. Cuff size is also important. The bladder should encircle and cover two-thirds of the length of the (upper) arm. The patient should be sitting upright in a chair with both feet flat on the floor for a minimum of five minutes prior to taking a reading. The patient should not be on any adrenergic stimulants, such as those found in many cold medications.

When taking manual measurements, the person taking the measurement should be careful to inflate the cuff suitably above anticipated systolic pressure. The person should inflate the cuff to 200 mmHg and then slowly release the air while palpating the radial pulse. After one minute, the cuff should be reinflated to 30 mmHg higher than the pressure at which the radial pulse was no longer palpable. A stethoscope should be placed lightly over the brachial artery. The cuff should be at the level of the heart and the cuff should be deflated at a rate of 2 to 3 mmHg/s. Systolic pressure is the pressure reading at the onset of the sounds described by Korotkoff (Phase one). Diastolic pressure is then recorded as the pressure at which the sounds disappear (K5) or sometimes the K4 point, where the sound is abruptly muffled. Two measurements should be made at least 5 minutes apart, and, if there is a discrepancy of more than 5 mmHg, a third reading should be done. The readings should then be averaged. An initial measurement should include both arms. In elderly patients who particularly when treated may show orthostatic hypotension, measuring lying sitting and standing BP may be useful. The BP should at some time have been measured in each arm, and the higher pressure arm preferred for subsequent measurements.

BP varies with time of day, as may the effectiveness of treatment, and archetypes used to record the data should include the time taken. Analysis of this is rare at present.

Automated machines are commonly used and reduce the variability in manually collected readings.^[25] Routine measurements done in medical offices of patients with known hypertension may incorrectly diagnose 20% of patients with uncontrolled hypertension^[26]

Home blood pressure monitoring can provide a measurement of a person's blood pressure at different times throughout the day and in different environments, such as at home and at work. Home monitoring may assist in the diagnosis of high or low blood pressure. It may also be used to monitor the effects of medication or lifestyle changes taken to lower or regulate blood pressure levels.

Home monitoring of blood pressure can also assist in the diagnosis of white coat hypertension. The American Heart Association^[27] states, "You may have what's called 'white coat hypertension'; that means your blood pressure goes up when you're at the doctor's office. Monitoring at home will help you measure your true blood pressure and can provide your doctor with a log of blood pressure measurements over time. This is helpful in diagnosing and preventing potential health problems."

Some home blood pressure monitoring devices also make use of blood pressure charting software. These charting methods provide printouts for the patient's physician and reminders to take a blood pressure reading. However, a simple and cheap way is simply to manually record values with pen and paper, which can then be inspected by a doctor.

Systolic hypertension is defined as an elevated systolic blood pressure. If systolic blood pressure is elevated with a normal diastolic blood pressure, it is called isolated systolic hypertension. Systolic hypertension may be due to reduced compliance of the aorta with increasing age.^[28]

[edit] Distinguishing primary vs. secondary hypertension

Once the diagnosis of hypertension has been made it is important to attempt to exclude or identify reversible (secondary) causes.

Over 91% of adult hypertension has no clear cause and is therefore called essential/primary hypertension. Often, it is part of the metabolic "syndrome X" in patients with insulin resistance: it occurs in combination with diabetes mellitus (type 2), combined hyperlipidemia and central obesity.
Secondary hypertension is more common in preadolescent children, with most cases caused by renal disease. Primary or essential hypertension is more common in adolescents and has multiple risk factors, including obesity and a family history of hypertension.^[29]

[edit] Investigations commonly performed in newly diagnosed hypertension

Tests are undertaken to identify possible causes of secondary hypertension, and seek evidence for end-organ damage to the heart itself or the eyes (retina) and kidneys. Diabetes and raised cholesterol levels being additional risk factors for the development of cardiovascular disease are also tested for as they will also require management.

Blood tests commonly performed include:

Creatinine (renal function) - to identify both underlying renal disease as a cause of hypertension and conversely hypertension causing onset of kidney damage. Also a baseline for later monitoring the possible side-effects of certain antihypertensive drugs.
Electrolytes (sodium, potassium)
Glucose - to identify diabetes mellitus
Cholesterol

Additional tests often include:

Testing of urine samples for proteinuria - again to pick up underlying kidney disease or evidence of hypertensive renal damage.
Electrocardiogram (EKG/ECG) - for evidence of the heart being under strain from working against a high blood pressure. Also may show resulting thickening of the heart muscle (left ventricular hypertrophy) or of the occurrence of previous silent cardiac disease (either subtle electrical conduction disruption or even a myocardial infarction).
Chest X-ray - again for signs of cardiac enlargement or evidence of cardiac failure.

[edit] Prevention

The degree to which hypertension can be prevented depends on a number of features including: current blood pressure level, changes in end/target organs (retina, kidney, heart - among others), risk factors for cardiovascular diseases and the age at presentation. Unless the presenting patient has very severe hypertension, there should be a relatively prolonged assessment period within which should be repeated measurements of blood pressure. Following this, lifestyle advice and non-pharmacological options should be offered to the patient, before any initiation of drug therapy.

The process of managing hypertension according the the guidelines of the British Hypertension Society suggest that non-pharmacological options should be explored in all patients who are hypertensive or pre-hypertensive. These measures include;

Weight reduction and regular aerobic exercise (e.g., walking) are recommended as the first steps in treating mild to moderate hypertension. Regular exercise improves blood flow and helps to reduce resting heart rate and blood pressure.^[30] Several studies indicate that low intensity exercise may be more effective in lowering blood pressure than higher intensity exercise.^[31] These steps are highly effective in reducing blood pressure, although drug therapy is still necessary for many patients with moderate or severe hypertension to bring their blood pressure down to a safe level.
Reducing dietary sugar intake
Reducing sodium (salt) in the diet may be effective: It decreases blood pressure in about 33% of people (see above). Many people use a salt substitute to reduce their salt intake.
Additional dietary changes beneficial to reducing blood pressure includes the DASH diet (dietary approaches to stop hypertension), which is rich in fruits and vegetables and low-fat or fat-free dairy foods. This diet has been shown to be effective based on research sponsored by the National Heart, Lung, and Blood Institute.^[32] In addition, an increase in daily calcium intake has the benefit of increasing dietary potassium, which theoretically can offset the effect of sodium and act on the kidney to decrease blood pressure. This has also been shown to be highly effective in reducing blood pressure.
Discontinuing tobacco use and alcohol consumption has been shown to lower blood pressure. The exact mechanisms are not fully understood, but blood pressure (especially systolic) always transiently increases following alcohol or nicotine consumption. Besides, abstention from cigarette smoking is important for people with hypertension because it reduces the risk of many dangerous outcomes of hypertension, such as stroke and heart attack. Note that coffee drinking (caffeine ingestion) also increases blood pressure transiently but does not produce chronic hypertension.
Reducing stress, for example with relaxation therapy, such as meditation and other mindbody relaxation techniques,^[33] by reducing environmental stress such as high sound levels and over-illumination can be an additional method of ameliorating hypertension. Jacobson's Progressive Muscle Relaxation and biofeedback are also used,^[34] particularly, device-guided paced breathing,^[35]^[36] although meta-analysis suggests it is not effective unless combined with other relaxation techniques.^[37]

[edit] Treatment

Main article: Antihypertensive

Unless hypertension is severe, lifestyle changes such as those discussed in the preceding section are strongly recommended before initiation of drug therapy. Adoption of the DASH diet is one example of lifestyle change repeatedly shown to effectively lower mildly-elevated blood pressure. If hypertension is high enough to justify immediate use of medications, lifestyle changes are initiated concomitantly.

There are many classes of medications for treating hypertension, together called antihypertensives, which — by varying means — act by lowering blood pressure. Evidence suggests that reduction of the blood pressure by 5-6 mmHg can decrease the risk of stroke by 40%, of coronary heart disease by 15%-20%, and reduces the likelihood of dementia, heart failure, and mortality from vascular disease.

The aim of treatment should be blood pressure control to <140/90 id="cite_ref-37" class="reference">[38] Each added drug may reduce the systolic blood pressure by 5-10 mmHg, so often multiple drugs are necessary to achieve blood pressure control.

Commonly used drugs include:

ACE inhibitors such as creatine captopril, enalapril, fosinopril (Monopril), lisinopril (Zestril), quinapril, ramipril (Altace)
Angiotensin II receptor antagonists: eg, telmisartan (Micardis, Pritor), irbesartan (Avapro), losartan (Cozaar), valsartan (Diovan), candesartan (Amias)
Alpha blockers such as prazosin, or terazosin. Doxazosin has been shown to increase risk of heart failure, and to be less effective than a simple diuretic,^[39] so is not recommended.
Beta blockers such as atenolol, labetalol, metoprolol (Lopressor, Toprol-XL), propranolol.
Calcium channel blockers such as nifedipine (Adalat)^[40] amlodipine (Norvasc), diltiazem, verapamil
Direct renin inhibitors such as aliskiren (Tekturna)
Diuretics: eg, bendroflumethiazide, chlortalidone, hydrochlorothiazide (also called HCTZ)
Combination products (which usually contain HCTZ and one other drug)

[edit] Choice of initial medication

Unless the blood pressure is severely elevated, consensus guidelines call for medically-supervised lifestyle changes and observation before recommending initiation of drug therapy. All drug treatments have side effects, and while the evidence of benefit at higher blood pressures is overwhelming, drug trials to lower moderately-elevated blood pressure have failed to reduce overall death rates.

If lifestyle changes are ineffective or the presenting blood pressure is critical, then drug therapy is initiated, often requiring more than one agent to effective lower hypertension. Which type of many medications should be used initially for hypertension has been the subject of several large studies and various national guidelines.

The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) study showed better cost-effectiveness and slightly better outcomes for the thiazide diuretic chlortalidone compared with a calcium channel blocker and an ACE inhibitor in a 33,357-member ethnically mixed study group.^[41] The 1993 consensus recommendation for use of thiazide diuretics as initial treatment stems in part from the ALLHAT study results, which concluded in 2002 that "Thiazide-type diuretics are superior in preventing 1 or more major forms of CVD and are less expensive. They should be preferred for first-step antihypertensive therapy."^[41]

A subsequent smaller study (ANBP2) did not show the slight advantages in thiazide diuretic outcomes observed in the ALLHAT study, and actually showed slightly better outcomes for ACE-inhibitors in older white male patients.^[42]

Thiazide diuretics are effective, recommended as the best first-line drug for hypertension by many experts, and much more affordable than other therapies, yet they are not prescribed as often as some newer drugs. Arguably, this is partly because they are off-patent, less profitable, and thus rarely promoted by the drug industry.^[43]

The consensus recommendations of thiazide diuretics as first-line therapy for hypertension stand against the backdrop that all blood pressure treatments have side-effects. Potentially serious side effects of the thiazide diuretics include hypercholesterolemia, and impaired glucose tolerance with consequent increased risk of developing Diabetes mellitus type 2. The thiazide diuretics also deplete circulating potassium unless combined with a potassium-sparing diuretic or supplemental potassium. On this basis, the consensus recommendations to prefer use of thiazides as first line treatment for essential hypertension have been repeatedly and strongly questioned.^[44]^[45]^[46] However as the Merck Manual of Geriatrics notes, "thiazide-type diuretics are especially safe and effective in the elderly."^[47]

[edit] Prognosis

It is based upon several factors including genetics, dietary habits, and overall lifestyle choices. If an individual conscious of their condition takes the necessary preventative measures to lower their blood pressure, they are more likely to have a much better outcome than someone who does not.

[edit] Complications

Diagram illustrating the main complications of persistent high blood pressure.

While elevated blood pressure alone is not an illness, it often requires treatment due to its short- and long-term effects on many organs. The risk is increased for:

Cerebrovascular accident (CVAs or strokes)
Myocardial infarction (heart attack)
Hypertensive cardiomyopathy (heart failure due to chronically high blood pressure)
Hypertensive retinopathy - damage to the retina
Hypertensive nephropathy - chronic renal failure due to chronically high blood pressure
Hypertensive encephalopathy - confusion, headache, convulsion due to vasogenic edema in brain due to high blood pressure.

[edit] Epidemiology

The level of blood pressure regarded as deleterious has been revised down during years of epidemiological studies. A widely quoted and important series of such studies is the Framingham Heart Study carried out in an American town: Framingham, Massachusetts. The results from Framingham and of similar work in Busselton, Western Australia have been widely applied. To the extent that people are similar this seems reasonable, but there are known to be genetic variations in the most effective drugs for particular sub-populations. Recently (2004), the Framingham figures have been found to overestimate risks for the UK population considerably. The reasons are unclear. Nevertheless the Framingham work has been an important element of UK health policy.

[edit] Children and adolescents

As with adults, blood pressure is a variable parameter in children. It varies between individuals and within individuals from day to day and at various times of the day. The epidemic of childhood obesity, the risk of developing left ventricular hypertrophy, and evidence of the early development of atherosclerosis in children would make the detection of and intervention in childhood hypertension important to reduce long-term health risks; however, supporting data are lacking. Most childhood hypertension, particularly in preadolescents, is secondary to an underlying disorder. Renal parenchymal disease is the most common (60 to 70%) cause of hypertension. Adolescents usually have primary or essential hypertension, making up 85 to 95% of cases.^[48]

[edit] History

Sushruta (6th century BCE) explained hypertension in a manner which matches the modern symptoms of the disease.^[49]

Abortus

2009-02-15T16:14:00.000-08:00

Gugur kandungan atau aborsi (bahasa Latin: abortus) adalah berhentinya kehamilan sebelum usia kehamilan 20 minggu yang mengakibatkan kematian janin.

Apabila janin lahir selamat (hidup) sebelum 38 minggu namun setelah 20 minggu, maka istilahnya adalah kelahiran prematur.

Dalam ilmu kedokteran, istilah-istilah ini digunakan untuk membedakan aborsi:

Spontaneous abortion: gugur kandungan yang disebabkan oleh trauma kecelakaan atau sebab-sebab alami.
Induced abortion atau procured abortion: pengguguran kandungan yang disengaja. Termasuk di dalamnya adalah:
- Therapeutic abortion: pengguguran yang dilakukan karena kehamilan tersebut mengancam kesehatan jasmani atau rohani sang ibu, terkadang dilakukan sesudah pemerkosaan.
- Eugenic abortion: pengguguran yang dilakukan terhadap janin yang cacat.
- Elective abortion: pengguguran yang dilakukan untuk alasan-alasan lain.

Dalam bahasa sehari-hari, istilah "keguguran" biasanya digunakan untuk spontaneous abortion, sementara "aborsi" digunakan untuk induced abortion.

Pengaturan oleh pemerintah

Aborsi menurut Kitab Undang-undang Hukum Pidana adalah tindakan kriminal di Indonesia. Pasal-pasal KUHP yang mengatur hal ini adalah pasal 229, 341, 342, 343, 346, 347, 348, dan 349.

Menurut KUHP, aborsi adalah:

Pengeluaran hasil konsepsi pada setiap stadium perkembangannya sebelum masa kehamilan yang lengkap tercapai (38-40 minggu).
Pengeluaran hasil konsepsi sebelum janin dapat hidup diluar kandungan (berat kurang dari 500 gram atau kurang dari 20 minggu).Dari segi medikolegal maka istilah abortus, keguguran, dan kelahiran prematur mempunyai arti yang sama dan menunjukkan pengeluaran janin sebelum usia kehamilan yang cukup.

[sunting] Jenis abortus menurut terjadinya

[sunting] Abortus spontanea (abortus yang berlangsung tanpa tindakan)

Yaitu:

Abortus imminens : Peristiwa terjadinya perdarahan dari uterus pada kehamilan sebelum 20 minggu, dimana hasil konsepsi masih dalam uterus, dan tanpa adanya dilatasi serviks.
Abortus insipiens : Peristiwa perdarahan uterus pada kehamilan sebelum 20 minggu dengan adanya dilatasi serviks uteri yang meningkat, tetapi hasil konsepsi masih dalam uterus.
Abortus inkompletus : Pengeluaran sebagian hasil konsepsi pada kehamilan sebelum 20 minggu dengan masih ada sisa tertinggal dalam uterus.
Abortus kompletus : Semua hasil konsepsi sudah dikeluarkan.

[sunting] Abortus provokatus (abortus yang sengaja dibuat)

Yaitu:

Menghentikan kehamilan sebelum janin dapat hidup di luar tubuh ibu. Pada umumnya dianggap bayi belum dapat hidup diluar kandungan apabila kehamilan belum mencapai umur 28 minggu, atau berat badanbayi belum 1000 gram, walaupun terdapat kasus bahwa bayi dibawah 1000 gram dapat terus hidup.

[sunting] Macam abortus provokatus

Abortus Provokatus Medisinalis/Artificialis/Therapeuticus

Di Indonesia yang dimaksud dengan indikasi medik adalah demi menyelamatkan nyawa ibu. Syarat-syaratnya:

Dilakukan oleh tenaga kesehatan yang memiliki keahlian dan kewenangan untuk melakukannya (yaitu seorang dokter ahli kebidanan dan penyakit kandungan) sesuai dengan tanggung jawab profesi.
Harus meminta pertimbangan tim ahli (ahli medis lain, agama, hukum, psikologi).
Harus ada persetujuan tertulis dari penderita atau suaminya atau keluarga terdekat.
Dilakukan di sarana kesehatan yang memiliki tenaga/peralatan yang memadai, yang ditunjuk oleh pemerintah.
Prosedur tidak dirahasiakan.
Dokumen medik harus lengkap.

Abortus Provokatus Kriminalis

Aborsi yang sengaja dilakukan tanpa adanya indikasi medik (ilegal). Biasanya pengguguran dilakukan dengan menggunakan alat-alat atau obat-obat tertentu.

[sunting] Penyebab Abortus

[sunting] Maternal

[sunting] Penyebab dari segi Maternal

Penyebab secara umum:

Infeksi akut

virus, misalnya cacar, rubella, hepatitis.
Infeksi bakteri, misalnya streptokokus.
Parasit, misalnya malaria.

Infeksi kronis

Sifilis, biasanya menyebabkan abortus pada trimester kedua.
Tuberkulosis paru aktif.
Keracunan, misalnya keracunan tembaga, timah, air raksa, dll.
Penyakit kronis, misalnya :
Gangguan fisiologis, misalnya Syok, ketakutan, dll.
Trauma fisik.

Penyebab yang bersifat lokal:

Fibroid, inkompetensia serviks.
Radang pelvis kronis, endometrtis.
Retroversi kronis.
Hubungan seksual yang berlebihan sewaktu hamil, sehingga menyebabkan hiperemia dan abortus.

[sunting] Penyebab dari segi Janin

Kematian janin akibat kelainan bawaan.
Mola hidatidosa.
Penyakit plasenta dan desidua, misalnya inflamasi dan degenerasi.

[sunting] Alasan untuk melakukan tindakan Abortus Provokatus

[sunting] Abortus Provokatus Medisinalis

Abortus yang mengancam (threatened abortion) disertai dengan perdarahan yang terus menerus, atau jika janin telah meninggal (missed abortion).
Mola Hidatidosa atau hidramnion akut.
Infeksi uterus akibat tindakan abortus kriminalis.
Penyakit keganasan pada saluran jalan lahir, misalnya kanker serviks atau jika dengan adanya kehamilan akan menghalangi pengobatan untuk penyakit keganasan lainnya pada tubuh seperti kanker payudara.
Prolaps uterus gravid yang tidak bisa diatasi.
Telah berulang kali mengalami operasi caesar.
Penyakit-penyakit dari ibu yang sedang mengandung, misalnya penyakit jantung organik dengan kegagalan jantung, hipertensi, nephritis, tuberkulosis paru aktif, toksemia gravidarum yang berat.
Penyakit-penyakit metabolik, misalnya diabetes yang tidak terkontrol yang disertai komplikasi vaskuler, hipertiroid, dan lain-lain.
Epilepsi, sklerosis yang luas dan berat.
Hiperemesis gravidarum yang berat, dan chorea gravidarum.
Gangguan jiwa, disertai dengan kecenderungan untuk bunuh diri. Pada kasus seperti ini, sebelum melakukan tindakan abortus harus dikonsultasikan dengan psikiater.

[sunting] Abortus Provokatus Kriminalis

Abortus provokatus kriminalis sering terjadi pada kehamilan yang tidak dikehendaki. Ada beberapa alasan wanita tidak menginginkan kehamilannya:

Alasan kesehatan, di mana ibu tidak cukup sehat untuk hamil.
Alasan psikososial, di mana ibu sendiri sudah enggan/tidak mau untuk punya anak lagi.
Kehamilan di luar nikah.
Masalah ekonomi, menambah anak berarti akan menambah beban ekonomi keluarga.
Masalah sosial, misalnya khawatir adanya penyakit turunan, janin cacat.
Kehamilan yang terjadi akibat perkosaan atau akibat incest (hubungan antar keluarga).
Selain itu tidak bisa dilupakan juga bahwa kegagalan kontrasepsi juga termasuk tindakan kehamilan yang tidak diinginkan.

[sunting] Pelaku Abortus Provokatus Kriminalis

Pelaku Abortus Provokatus Kriminalis biasanya adalah:

Wanita bersangkutan.
Dokter atau tenaga medis lain (demi keuntungan atau demi rasa simpati).
Orang lain yang bukan tenaga medis (misalnya dukun.

[sunting] Akibat Abortus Provokatus Kriminalis

[sunting] Komplikasi medis yang dapat timbul pada ibu

[sunting] Perforasi

Dalam melakukan dilatasi dan kerokan harus diingat bahwa selalu ada kemungkinan terjadinya perforasi dinding uterus, yang dapat menjurus ke rongga peritoneum, ke ligamentum latum, atau ke kandung kencing. Oleh sebab itu, letak uterus harus ditetapkan lebih dahulu dengan seksama pada awal tindakan, dan pada dilatasi serviks tidak boleh digunakan tekanan berlebihan. Kerokan kuret dimasukkan dengan hati-hati, akan tetapi penarikan kuret ke luar dapat dilakukan dengan tekanan yang lebih besar. Bahaya perforasi ialah perdarahan dan peritonitis. Apabila terjadi perforasi atau diduga terjadi peristiwa itu, penderita harus diawasi dengan seksama dengan mengamati keadaan umum, nadi, tekanan darah, kenaikan suhu, turunnya hemoglobin, dan keadaan perut bawah. Jika keadaan meragukan atau ada tanda-tanda bahaya, sebaiknya dilakukan laparatomi percobaan dengan segera.

[sunting] Luka pada serviks uteri

Apabila jaringan serviks keras dan dilatasi dipaksakan maka dapat timbul sobekan pada serviks uteri yang perlu dijahit. Apabila terjadi luka pada ostium uteri internum, maka akibat yang segera timbul ialah perdarahan yang memerlukan pemasangan tampon pada serviks dan vagina. Akibat jangka panjang ialah kemungkinan timbulnya incompetent cerviks.

[sunting] Pelekatan pada kavum uteri

Melakukan kerokan secara sempurna memerlukan pengalaman. Sisa-sisa hasil konsepsi harus dikeluarkan, tetapi jaringan miometrium jangan sampai terkerok, karena hal itu dapat mengakibatkan terjadinya perlekatan dinding kavum uteri di beberapa tempat. Sebaiknya kerokan dihentikan pada suatu tempat apabila pada suatu tempat tersebut dirasakan bahwa jaringan tidak begitu lembut lagi.

[sunting] Perdarahan

Kerokan pada kehamilan yang sudah agak tua atau pada mola hidatidosa terdapat bahaya perdarahan. Oleh sebab itu, jika perlu hendaknya dilakukan transfusi darah dan sesudah itu, dimasukkan tampon kasa ke dalam uterus dan vagina.

[sunting] Infeksi

Apabila syarat asepsis dan antisepsis tidak diindahkan, maka bahaya infeksi sangat besar. Infeksi kandungan yang terjadi dapat menyebar ke seluruh peredaran darah, sehingga menyebabkan kematian. Bahaya lain yang ditimbulkan abortus kriminalis antara lain infeksi pada saluran telur. Akibatnya, sangat mungkin tidak bisa terjadi kehamilan lagi.

[sunting] Lain-lain

Komplikasi yang dapat timbul dengan segera pada pemberian NaCl hipertonik adalah apabila larutan garam masuk ke dalam rongga peritoneum atau ke dalam pembuluh darah dan menimbulkan gejala-gejala konvulsi, penghentian kerja jantung, penghentian pernapasan, atau hipofibrinogenemia. Sedangkan komplikasi yang dapat ditimbulkan pada pemberian prostaglandin antara lain panas, rasa enek, muntah, dan diare.

Komplikasi yang Dapat Timbul Pada Janin: Sesuai dengan tujuan dari abortus itu sendiri yaitu ingin mengakhiri kehamilan, maka nasib janin pada kasus abortus provokatus kriminalis sebagian besar meninggal. Kalaupun bisa hidup, itu berarti tindakan abortus gagal dilakukan dan janin kemungkinan besar mengalami cacat fisik.

Secara garis besar tindakan abortus sangat berbahaya bagi ibu dan juga janin yaitu bisa menyebabkan kematian pada keduanya.

Cara – cara Abortus Provokatus Kriminalis Kekerasan Mekanik : 1. Umum

a. Latihan olahraga berlebihan

b. Naik kuda berlebihan

c. Mendaki gunung, berenang, naik turun tangga

d. Tekanan / trauma pada abdomen

Wanita cemas akan kehilangan kehamilannya karena olah raga yang berlebih dan mungkin kekerasan yang berpengaruh terhadap janinnya. Aktivitas hiruk pikuk, mengendarai kuda biasanya tidak efektif dan beberapa wanita mencari kekerasan dari suaminya. Meninju dan menendang perut sudah umum dan kematian akibat ruptur organ dalam seperti hati, limpa atau pencernaan, telah banyak dilaporkan. Ironisnya, uterus biasanya masih dalam kondisi baik.

2. Lokal

a. Memasukkan alat-alat yang dapat menusuk kedalam vagina : pensil, paku, jeruji sepeda

b. Alat merenda, kateter atau alat penyemprot untuk menusuk atau menyemprotkan cairan kedalam uterus untuk melepas kantung amnion

c. Alat untuk memasang IUD

d. Alat yang dapat dilalui arus listrik

e. Aspirasi jarum suntik

Metode hisapan sering digunakan pada aborsi yang merupakan cara yang ilegal secara medis walaupun dilakukan oleh tenaga medis. Tabung suntik yang besar dilekatkan pada ujung kateter yang dapat dilakukan penghisapan yang berakibat ruptur dari chorionic sac dan mengakibatkan abortus. Cara ini aman asalkan metode aseptic dijalankan, jika penghisapan tidak lengkap dan masih ada sisa dari hasil konsepsi maka dapat mengakibatkan infeksi.

Tujuan dari merobek kantong kehamilan adalah jika kantong kehamilan sudah rusak maka secara otomatis janin akan dikeluarkan oleh kontraksi uterus. Ini juga dapat mengakibatkan dilatasi saluran cerviks, yang dapat mengakhiri kehamilan. Semua alat dapat digunakan dari pembuka operasi sampai jari-jari dari ban sepeda. Paramedis yang melakukan abortus suka menggunakan kateter yang kaku. Jika digunakan oleh dokter maupun suster, yang melakukan mempunyai pengetahuan anatomi dan menggunakan alat yang steril maka resikonya semakin kecil. Akan tetapi orang awam tidak mengetahui hubungan antara uterus dan vagina. Alat sering digunakan dengan cara didorong ke belakang yang orang awam percayai bahwa keadaan cerviks di depan vagina. Permukaan dari vagina dapat menjadi rusak dan alat mungkin masuk ke usus bahkan hepar. Penetrasi dari bawah atau tengah vagina dapat juga terjadi perforasi. Jika cerviks dimasuki oleh alat, maka cerviks dapat ruptur dan alat mungkin masuk lewat samping. Permukaan luar dapat cedera dengan pengulangan, usaha yang ceroboh yang berusaha mengeluarkan benda yang terlalu tebal ke saluran yang tidak membuka. Jika sukses melewati saluran dari uterus, mungkin langsung didorong ke fundus, yang akan merusak peritoneal cavity. Bahaya dari penggunaan alat adalah pendarahan dan infeksi. Perforasi dari dinding vagina atau uterus dapat menyebabkan pendarahan, yang mungkin diakibatkan dari luar atau dalam. Sepsis dapat terjadi akibat penggunaan alat yang tidak steril atau kuman berasal dari vagina dan kulit. Bahaya yang lebih ringan(termasuk penggunaan jarum suntik) adalah cervical shock. Ini dapat membuat dilatasi cerviks, dalam keadaaan pasien yang tidak dibius, alat mungkin menyebabkan vagal refleks, yang melalui sistem saraf parasimpatis, yang dapat mengakibatkan cardiac arrest. Ini merupakan mekanisme yang berpotensi menimbulkan ketakutan yang dapat terjadi pada orang yang melakukan abortus kriminalis. Kekerasan Kimiawi / Obat-obatan atau Bahan-bahan yang Bekerja Pada Uterus Berbagai macam zat yang digunakan baik secara lokal maupun melalui mulut telah banyak digunakan untuk menggugurkan kandungan. Beberapa zat mempunyai efek yang baik sedangkan beberapa lainnya berbahaya. Zat yang digunakan secara lokal contohnya fenol dan lysol, merkuri klorida, potassium permagnat, arsenik, formaldehid, dan asam oxalat. Semua mempunyai bahaya sendiri, baik dari korosi lokal maupun efek sistemik jika diserap. Pseudomembran yang nekrotik mungkin berasal dari vagina dan kerusakan cerviks mungkin terjadi. Potasium permangat adalah zat yang muncul selama perang yang terakhir dan berlangsung beberapa tahun, 650 kasus dilaporkan hingga tahun 1959, yang parah hanya beberapa. Ini dapat menyebabkan nekrosis pada vagina jika diserap yang dapat mempunyai efek sistemik yang fatal termasuk kerusakan ginjal. Permanganat dapat menyebabkan pendarahan vagina dari nekrosis, yang mana dapat membahayakan janin

Jenis obat-obatan yang dipakai untuk menginduksi abortus antara lain. : a. Emmenagogum : obat untuk melancarkan haid Cara kerja : Indirect Congesti + engorgement mucosa ↓ Bleeding ↓ Kontraksi Uterus ↓ Foetus dikeluarkan

Direct : Bekerja langsung pada uterus/saraf motorik uterus.

Misal : Aloe, Cantharides (racun irritant), Caulopylin, Borax, Apiol, Potassium permanganate, Santonin, Senega, Mangan dioksida, dll.

b. Purgativa/Emetica :obat-obatan yang menimbulkan kontraksi GI tract

Misal :

Colocynth : Aloe

Castor oil : Magnesim sulfate, Sodium sulfate.

c. Ecbolica : menimbulkan kontraksi uterus secara langsung. Misal : Apiol, Ergot, Ergometrine, Extract secale, Extract pituatary, Pituitrine, Exytocin.

Cara kerja ergot : Merangsang alpha 1 receptor pada uterus

↓

Kontraksi uterus yang kuat dan lama

d. Garam dari logam : biasanya sebelum mengganggu kehamilannya sudah membahayakan keselamatan ibu. Dengan tujuan menimbulkan tonik kontraksi pada uterus. Misal : Arsenicum, HgCl, Potassium bichromate, Ferro sulfate, ferri chlorida

Diagnosis kehamilan ditegakkan atas dasar adanya tanda kehamilan. Tanda kehamilan dibagi menjadi 2 yakni : 1. Tanda pasti 2. Tanda tidak pasti i. Tanda mungkin (probable signs) ii. Tanda dugaan (presumptive signs)

Tanda Pasti Tanda pasti kehamilan antara lain : 1. Pada inspeksi didapatkan gerakan janin pada minggu ke 16-18. 2. Pada palpasi didapatkan gerakan janin dan teraba bagian-bagian janin pada minggu ke 20. 3. Pada auskultasi didapatkan detak jantung janin pada miggu ke 18-20. 4. Pada pemeriksaan Rontgen didapatkan kerangka fetus pada minggu ke 16. 5. Pada pemeriksaan USG didapatkan gestasional sac pada minggu ke 4.

Tanda mungkin (probable signs) Tanda mungkin kehamilan antara lain : 1. Pembesaran perut dan uterus. 2. Perlunakan serviks dan serviks-uterus (Tanda Piscaseck) 3. Kontraksi uterus (Braxton Hicks) 4. Ballotment (palpasi kepala janin) 5. Tes hormon β-HCG urine, kadar β-HCG urine maksimal pada minggu 5-18.

Tanda dugaan (Presumptive signs) Tanda dugaan kehamilan antara lain : 1. Amenore 2. Nausea-Vomiting 3. Malaise 4. Polakisuria 5. Hiperpigmentasi kulit 6. Striae gravidarum 7. Kebiruan pada serviks dan vagina (Tanda Chadwick) 8. Payudara : hipertrofi mammae, hiperpigmentasi areola, hipertrofi kelenjar Montgomery, kolostrum (mingggu ke 12).

Tinggi fundus uteri sesuai usia kehamilan Uterus pada wanita tidak hamil kira-kira sebesar telur ayam. Pada palpasi tidak dapat diraba. Pada kehanilan uterus tumbuh secara teratur, kecuali jika ada gangguan pada kehamilan tersebut. Perkiraan tinggi fundus uteri sesuai usia kehamilan : 1. Kehamilan usia 12 minggu : tepat di atas simfisis (syarat pemeriksaan vesica urinaria dikosongkan dahulu). 2. Kehamilan usia 16 minggu : setengah jarak simfisis ke pusat. 3. Kehamilan usia 20 minggu : tepi bawah pusat. 4. Kehamilan usia 24 minggu : tepi atas pusat. 5. Kehamilan usia 28 minggu : sepertiga jarak pusat ke processus xyphoideus atau 3 jari di atas pusat. 6. Kehamilan usia 32 minggu : setengah jarak pusat ke processus xyphoideus. 7. Kehamilan usia 36 minggu : pada 1 jari bawah processus xyphoideus.

    b. Tanda-tanda post Partus ( Masa Puperium )

Masa puerpurium atau masa nifas mulai setelah partus selesai, dan berakhir setelah kira-kira 6 minggu. Akan tetapi, seluruh alat genital baru pulih kembali seperti sebelum ada kehamilan dalam waktu 3 bulan.

Aspek Hukum dan Medikolegal Abortus Povocatus Criminalis Abortus telah dilakukan oleh manusia selama berabad-abad, tetapi selama itu belum ada undang-undang yang mengatur mengenai tindakan abortus. Peraturan mengenai hal ini pertama kali dikeluarkan pada tahun 4 M di mana telah ada larangan untuk melakukan abortus. Sejak itu maka undang-undang mengenai abortus terus mengalami perbaikan, apalagi dalam tahun-tahun terakhir ini di mana mulai timbul suatu revolusi dalam sikap masyarakat dan pemerintah di berbagai negara di dunia terhadap tindakan abortus. Hukum abortus di berbagai negara dapat digolongkan dalam beberapa kategori sebagai berikut:

• Hukum yang tanpa pengecualian melarang abortus, seperti di Belanda.

• Hukum yang memperbolehkan abortus demi keselamatan kehidupan penderita (ibu), seperti di Perancis dan Pakistan.

• Hukum yang memperbolehkan abortus atas indikasi medik, seperti di Kanada, Muangthai dan Swiss.

• Hukum yang memperbolehkan abortus atas indikasi sosio-medik, seperti di Eslandia, Swedia, Inggris, Scandinavia, dan India.

• Hukum yang memperbolehkan abortus atas indikasi sosial, seperti di Jepang, Polandia, dan Yugoslavia.

• Hukum yang memperbolehkan abortus atas permintaan tanpa memperhatikan indikasi-indikasi lainnya (Abortion on requst atau Abortion on demand), seperti di Bulgaris, Hongaria, USSR, Singapura.

• Hukum yang memperbolehkan abortus atas indikasi eugenistis (aborsi boleh dilakukan bila fetus yang akan lahir menderita cacat yang serius) misalnya di India

• Hukum yang memperbolehkan aborsi atas indikasi humanitarian (misalnya bila hamil akibat perkosaan) seperti di Jepang

Negara-negara yang mengadakan perubahan dalam hukum abortus pada umumnya mengemukakan salah satu alasan/tujuan seperti yang tersebut di bawah ini:

• Untuk memberikan perlindungan hukum pada para medisi yang melakukan abortus atas indikasi medik.

• Untuk mencegah atau mengurangi terjadinya abortus provocatus criminalis.

• Untuk mengendalikan laju pertambahan penduduk.

• Untuk melindungi hal wanita dalam menentukan sendiri nasib kandungannnya.

• Untuk memenuhi desakan masyarakat.

Di Indonesia, baik menurut pandangan agama, Undang-Undang Negara, maupun Etik Kedokteran, seorang dokter tidak diperbolehkan untuk melakukan tindakan pengguguran kandungan (abortus provokatus). Bahkan sejak awal seseorang yang akan menjalani profesi dokter secara resmi disumpah dengan Sumpah Dokter Indonesia yang didasarkan atas Deklarasi Jenewa yang isinya menyempurnakan Sumpah Hippokrates, di mana ia akan menyatakan diri untuk menghormati setiap hidup insani mulai dari saat pembuahan. Dari aspek etika, Ikatan Dokter Indonesia telah merumuskannya dalam Kode Etik Kedokteran Indonesia mengenai kewajiban umum, pasal

7d: Setiap dokter harus senantiasa mengingat akan kewajiban melindungi hidup makhluk insani. Pada pelaksanaannya, apabila ada dokter yang melakukan pelanggaran, maka penegakan implementasi etik akan dilakukan secara berjenjang dimulai dari panitia etik di masing-masing RS hingga Majelis Kehormatan Etika Kedokteran (MKEK). Sanksi tertinggi dari pelanggaran etik ini berupa "pengucilan" anggota dari profesi tersebut dari kelompoknya. Sanksi administratif tertinggi adalah pemecatan anggota profesi dari komunitasnya.

Ditinjau dari aspek hukum, pelarangan abortus justru tidak bersifat mutlak. Abortus buatan atau abortus provokatus dapat digolongkan ke dalam dua golongan yakni: 1. Abortus buatan legal Yaitu pengguguran kandungan yang dilakukan menurut syarat dan cara-cara yang dibenarkan oleh undang-undang. Populer juga disebut dengan abortus provocatus therapeticus, karena alasan yang sangat mendasar untuk melakukannya adalah untuk menyelamatkan nyawa ibu. Abortus atas indikasi medik ini diatur dalam Undang Undang Republik Indonesia Nomor 23 Tahun 1992 tentang Kesehatan:

PASAL 15: 1) Dalam keadaan darurat sebagai upaya untuk menyelamatkan jiwa ibu hamil dan atau janinnya, dapat dilakukan tindakan medis tertentu. 2) Tindakan medis tertentu sebagaimana dimaksud dalam ayat(1) hanya dapat dilakukan: a. Berdasarkan indikasi medis yang mengharuskan diambilnya tindakan tersebut; b. Oleh tenaga kesehatan yang mempunyai keahlian dan kewenangan untuk itu dan dilakukan sesuai dengan tanggung jawab profesi serta berdasarkan pertimbangan tim ahli; c. Dengan persetujuan ibu hamil yang bersangkutan atau suami atau keluarganya; d. Pada sarana kesehatan tertentu. 3) Ketentuan lebih lanjut mengenai tindakan medis tertentu sebagaimana dimaksud dalam ayat (1) dan ayat (2) ditetapkan dengan Peraturan Pemerintah.

Pada penjelasan UU no 23 tahun 1992 pasal 15 dinyatakan sebagai berikut: Ayat (1) : Tindakan medis dalam bentuk pengguguran kandungan dengan alasan apapun, dilarang karena bertentangan dengan norma hukum, norma agama, norma kesusilaan dan norma kesopanan. Namun dalam keadaan darurat sebagai upaya untuk menyelamatkan jiwa ibu atau janin yang dikandungnya dapat diambil tindakan medis tertentu Ayat (2) Butir a : Indikasi medis adalah suatu kondisi yang benar-benar mengharuskan diambil tindakan medis tertentu sebab tanpa tindakan medis tertentu itu,ibu hamil dan janinnya terancam bahaya maut. Butir b : Tenaga kesehatan yang dapat melakukan tindakan medis tertentu adalah tenaga yang memiliki keahlian dan wewenang untuk melakukannya yaitu seorang dokter ahli kandungan seorang dokter ahli kebidanan dan penyakit kandungan. Butir c : Hak utama untuk memberikan persetujuan ada ibu hamil yang bersangkutan kecuali dalam keadaan tidak sadar atau tidak dapat memberikan persetujuannya ,dapat diminta dari semua atau keluarganya. Butir d : Sarana kesehatan tertentu adalah sarana kesehatan yang memiliki tenaga dan peralatan yang memadai untuk tindakan tersebut dan ditunjuk oleh pemerintah. Ayat (3) : Dalam Peraturan Pemerintah sebagai pelaksanan dari pasal ini dijabarkan antara lain mengenal keadaan darurat dalam menyelamatkan jiwa ibu hamil atau janinnya,tenaga kesehatan mempunyai keahlian dan wewenang bentuk persetujuan, sarana kesehatan yang ditunjuk. 2. Abortus Provocatus Criminalis ( Abortus buatan illegal ) Yaitu pengguguran kandungan yang tujuannya selain untuk menyelamatkan atau menyembuhkan si ibu, dilakukan oleh tenaga yang tidak kompeten serta tidak memenuhi syarat dan cara-cara yang dibenarkan oleh undang-undang. Abortus golongan ini sering juga disebut dengan abortus provocatus criminalis karena di dalamnya mengandung unsur kriminal atau kejahatan. Beberapa pasal yang mengatur abortus provocatus dalam Kitab Undang-undang Hukum Pidana (KUHP):

PASAL 299 1) Barang siapa dengan sengaja mengobati seorang wanita atau menyuruh supaya diobati, dengan diberitahukan atau ditimbulkan harapan, bahwa karena pengobatan itu hamilnya dapat digugurkan, diancam dengan pidana penjara paling lama empat tahun atau denda paling banyak empat pulu ribu rupiah. 2) Jika yang bersalah, berbuat demikian untuk mencari keuntungan, atau menjadikan perbuatan tersebut sebagai pencaharian atau kebiasaan atau jika dia seorang tabib, bidan atau juru obat, pidananya dapat ditambah sepertiga. 3) Jika yang bersalah melakukan kejahatan tersebut dalam menjalankan pencaharian, maka dapat dicabut haknya untuk melakukan pencaharian.

PASAL 346 Seorang wanita yang sengaja menggugurkan atau mematikan kandungannya atau menyuruh orang lain untuk itu, diancam dengan pidana penjara paling lama empat tahun.

PASAL 347 1) Barang siapa dengan sengaja menggugurkan atau mematikan kandungan seorang wanita tanpa persetujuan, diancam dengan pidana penjara paling lama dua belas tahun. 2) Jika perbuatan itu menyebabkan matinya wanita tersebut, dikenakan pidana penjara paling lama lima belas tahun.

PASAL 348 1) Barang siapa dengan sengaja menggugurkan atau mematikan kandungan seseorang wanita dengan persetujuannya, diancam dengan pidana penjara paling lama lima tahun enam bulan. 2) Jika perbuatan tersebut mengakibatkan matinya wanita tersebut, dikarenakan pidana penjara paling lama tujuh tahun.

PASAL 349 Jika seorang dokter, bidan atau juru obat membantu melakukan kejahatan yang tersebut pasal 346, ataupun melakukan atau membantu melakukan salah satu kejahatan yang diterangkan dalam pasal 347 dan 348, maka pidana yang ditentukan dalam pasal itu dapat ditambah dengn sepertiga dan dapat dicabut hak untuk menjalankan pencaharian dalam mana kejahatan dilakukan.

PASAL 535 Barang siapa secara terang-terangan mempertunjukkan suatu sarana untuk menggugurkan kandungan, maupun secara terang-terangan atau tanpa diminta menawarkan, ataupun secara terang-terangn atau dengan menyiarkan tulisan tanpa diminta, menunjuk sebagai bisa didapat, sarana atau perantaraan yang demikian itu, diancam dengan kurungan paling lama tiga bulan atau denda paling banyak empat ribu lima ratus rupiah. Dari rumusan pasal-pasal tersebut diatas dapat ditarik kesimpulan : 1. Seorang wanita hamil yang sengaja melakukan abortus atau ia menyuruh orang lain, diancam hukuman empat tahun. 2. Seseorang yang sengaja melakukan abortus terhadap ibu hamil, dengan tanpa persetujuan ibu hamil tersebut diancam hukuman 12 tahun, dan jika ibu hamil itu mati diancam 15 tahun 3. Jika dengan persetujuan ibu hamil, maka diancam hukuman 5,5 tahun penjara dan bila ibu hamil tersebut mati diancam hukuman 7 tahun penjara. 4. Jika yang melakukan dan atau membantu melakukan abortus tersebut seorang dokter, bidan atau juru obat (tenaga kesehatan) ancaman hukumannya ditambah sepertiganya dan hak untuk praktek dapat dicabut. Meskipun dalam KUHP tidak terdapat satu pasal pun yang memperbolehkan seorang dokter melakukan abortus atas indikasi medik, sekalipun untuk menyelamatkan jiwa ibu, dalam prakteknya dokter yang melakukannya tidak dihukum bila ia dapat mengemukakan alasan yang kuat dan alasan tersebut diterima oleh hakim (Pasal 48). Selain KUHP, abortus buatan yang ilegal juga diatur dalam Undang Undang Republik Indonesia Nomor 23 Tahun 1992 tentang Kesehatan:

PASAL 80 Barang siapa dengan sengaja melakukan tindakan medis tertentu terhadap ibu hamil yang tidak memenuhi ketentuan sebagaimana dimaksud dalam pasal 15 ayat (1) dan ayat (2), dipidana dengan penjara paling lama 15 (lima belas) tahun dan pidana denda paling banyak Rp. 500.000.000,00 (lima ratus juta rupiah)

SLE

2009-02-15T16:08:00.000-08:00

Introduction

Background

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease of unknown cause that affects multiple organ systems. Immunologic abnormalities, especially the production of a number of antinuclear antibodies, are another prominent feature of this disease. The clinical course is marked by spontaneous remissions and relapses. Its multisystemic manifestations and the complications from the use of immunosuppressive agents make the diagnosis and management of this entity challenging.

Pathophysiology

Autoantibodies, circulating immune complexes, and T lymphocytes all contribute to the expression of disease. Organ systems affected include dermatologic, serous membranes, renal, central nervous system (CNS), hematologic, musculoskeletal, cardiovascular, pulmonary, vascular endothelium, and gastrointestinal. The diagnosis of SLE is made if 4 or more of the following manifestations are present, either serially or simultaneously (specificity, 95%; sensitivity, 75%):

Malar rash
Discoid rash
Photosensitivity
Oral ulcers
Arthritis
Serositis
Renal disorder
Neurologic disorder
Hematologic disorder
Immunologic disorder
Antinuclear antibody

Frequency

United States

In the United States, the annual incidence of SLE ranges from 6-35 per 100,000 population. The incidence of SLE in black women is approximately 4 times higher than in white women. SLE is more frequent in Asian women as well.

The reported prevalence of SLE in the population is 40-50 cases per 100,000 population.

International

In England, the incidence is 200 cases per 100,000 women (aged 18-65 y).

Mortality/Morbidity

Recent studies in Europe and Canada have shown a gradual increase in mortality the longer the patient has the disease, from greater than 90% of patients surviving more than 5 years to 10-year and 20-year survival rates of 75-85% and 70%, respectively.

Early deaths usually are caused by active disease. Atherosclerosis is a leading cause in late deaths. Infection and nephritis are major causes of mortality in all stages of SLE.
After dialysis or transplantation, a reduction in disease activity and flares has been reported.
Thrombosis, often secondary to antiphospholipid syndrome and a hypercoagulable state, carditis, pneumonitis, pulmonary hypertension, stroke, myocardial infarction, and cerebritis cause severe morbidity and mortality.

Race

The prevalence of SLE is higher among Asians, African Americans, African Caribbeans, Hispanic Americans, and Asian Indians in Great Britain. In comparison, SLE occurs infrequently in blacks in Africa.

In New Zealand, the prevalence and mortality of SLE are higher in Polynesians than in whites.

In France, SLE is more common among immigrants from Spain, Portugal, North Africa, and Italy.

Sex

The frequency of SLE among women is increased and has been attributed to an estrogen hormonal effect.

In children in whom sex hormone effects are presumably minimal, the female-to-male ratio is 3:1. In adults, the female-to-male ratio ranges from 10-15:1. In older individuals, the female-to-male ratio is approximately 8:1.

Age

Sixty-five percent of patients with SLE have disease onset between the ages of 16 and 55 years. Of the remaining cases, 20% present before age 16 years and 15% after age 55 years.

Clinical

History

Manifestations are diverse, and the mean length of time between onset of symptoms and diagnosis is 5 years. The disease is characterized by exacerbations and remissions. Many women relate flares of their lupus to the postovulatory phase of the menstrual cycle, with resolution of symptoms at the time of menses.

Constitutional symptoms include low-grade fever, fatigue, malaise, anorexia, nausea, and weight loss. The initial presentation may involve one or more organ systems.
Arthralgia occurs in more than 90% of the patients and is the initial complaint in many patients. Often, the pain is out of proportion to physical findings.
A malar, butterfly rash over the cheeks and bridge of the nose (55-90%) with photosensitivity to ultraviolet (UV) light has been reported (mostly in whites). It also often involves the chin and ears. It lasts for a few days and tends to recur.
Painful or painless ulcers in the nose and mouth are frequent complaints. Perforation of the nasal septum occurs infrequently.
Neurologic symptoms include mild cognitive defects, organic brain syndromes, delirium, psychosis, seizures, headache, and/or neuropathies. Any region of the brain, meninges, spinal cord, and cranial and peripheral nerves can be involved. CNS events often occur when SLE is active in other organ systems.
Psychosis, related to SLE or to high-dose steroids, is one of the psychiatric manifestations of SLE. If the psychosis is unaffected after stopping the steroid, then it is most likely related to the disease process.
Pleuritic pain, dyspnea, cough, fever, and chest pain are important cardiopulmonary complaints.
Patients may present with abdominal pain, diarrhea, and vomiting. Intestinal perforation and vasculitis are important diagnoses to exclude.
A number of other conditions seen more frequently with SLE include the following:
- Stroke
- Pulmonary embolus
- Deep venous thrombosis (DVT)
- Acute ischemia
- Retinal vasculitis

Physical

Fever is a challenging problem in systemic lupus erythematosus (SLE). It can be a manifestation of active lupus or a representation of infection, malignancy, or drug reaction. Temperature higher than 102°F should prompt a search for infection. Lower-grade temperature is observed in patients on immunosuppressive agents.
Malar rash is a fixed erythema that spares the nasolabial folds. It is a butterfly rash that can be flat or raised over the cheeks and bridge of the nose. It also often involves the chin and ears.
Discoid rash occurs in 20% of patients with SLE and can result in disfiguring scars. The discoid rash can present as erythematous patches with keratotic scaling over sun-exposed areas of the skin. Systemic manifestations of SLE may be absent.
Alopecia or loss or loss of hair may occur.
All patients experience painless or painful oral or vaginal ulcers, which are helpful in making the diagnosis, during the course of their illness.
Gastrointestinal findings include vague abdominal discomfort, nausea, and diarrhea. Acute crampy abdominal pain, vomiting, and diarrhea may signify vasculitis of the intestine.
Joint findings
- Tenderness, edema, and effusions accompany a polyarthritis that is symmetric, nonerosive, and usually nondeforming. The arthritis frequently involves the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of the hands as well as the wrists and knees.
- Consider avascular necrosis, which is common in patients who are taking glucocorticoids.
- In addition, consider septic arthritis when one joint is inflamed out of proportion to all other joints.
Central nervous system findings
- All types of seizures have been reported; the most frequent is the grand mal seizure. Sensory or sensorimotor neuropathies are also common.
- Incidence of stroke is high in the first 5 years of disease. Patients with antiphospholipid antibodies are at higher risk for such events.
Funduscopic examination is important in patients with visual complaints. Retinal vasculitis can lead to blindness and is demonstrated by sheathed narrow retinal arterioles with white exudates adjacent to the vessels.
The renal system can be affected leading to renal failure. Specific signs and symptoms of renal disease may not be apparent until advanced nephrotic syndrome or renal failure is present; therefore, obtaining a urine analysis and serum BUN and creatinine levels on a regular basis is important.
Cardiovascular system findings
- Atherosclerosis occurs prematurely in patients with SLE and is an independent risk factor for cardiovascular disease.
- Pulmonary hypertension, vasculitis with digital infarcts, and splinter hemorrhages may be observed.
- Systolic murmurs are reported in up to 70% of cases. They may be secondary to fever, hypoxia, anemia, or Libman-Sacks endocarditis (associated with antiphospholipid antibodies).
- Pericarditis has an incidence of 20-30% and is the most common presentation of heart involvement. It is usually associated with small effusions, but it may involve larger effusions when uremia is concomitant. Myocarditis can cause heart failure, arrhythmias, and sudden death.
Pulmonary findings
- Tachypnea, cough, and fever are common manifestations of lupus pneumonitis.
- Hemoptysis may signify pulmonary hemorrhage secondary to the disease. However, infection is the most common cause of infiltrates seen on radiographs.

Causes

Many of the clinical manifestations of SLE are caused by the effects of circulating immune complexes on various tissues or to the direct effects of antibodies to cell surface components.
Whether polyclonal B-cell activation or a response to specific antigens exists is unclear.
Cytotoxic T cells and suppressor T cells (which would normally downregulate immune responses) are decreased.
The generation of polyclonal T-cell cytolytic activity is impaired.
Helper (CD4⁺) T cells are increased.
A lack of immune tolerance is observed in animal models.
A high concordance rate (14-57%) of SLE is noted in monozygotic twins. Each patient manifests his or her disease differently.
Five to twelve percent of relatives of patients with SLE have the disease.
If a mother has SLE, her daughter's risk of developing the disease is 1:40, and her son's risk is 1:250.
Administration of estrogen to postmenopausal women appears to double the risk of developing SLE.
Breastfeeding is associated with a decreased risk of developing SLE.
Viruses, for example, may stimulate specific cells in the immune network. Patients with SLE also have higher titers of antibodies to Epstein-Barr virus (EBV), have increased circulating EBV viral loads, and make antibodies to retroviruses, including to protein regions homologous to nuclear antigens.
Trypanosomiasis or mycobacterial infections may induce anti-DNA antibodies or even lupuslike symptoms, and lupus flares may follow bacterial infections.
Silica dust and cigarette smoking may increase the risk of developing SLE.
Photosensitivity is clearly a precipitant of skin disease.
The presence of antiphospholipid antibodies in patients dictates a constellation of signs caused by thrombosis.

Pielonefritis

2009-02-15T16:07:00.001-08:00

DEFINISI
Pielonefritis adalah infeksi bakteri pada salah satu atau kedua ginjal.

PENYEBAB
Escherichia coli (bakteri yang dalam keadaan normal ditemukan di usus besar) merupakan penyebab dari 90% infeksi ginjal diluar rumah sakit dan penyebab dari 50% infeksi ginjal di rumah sakit.
Infeksi biasanya berasal dari daerah kelamin yang naik ke kandung kemih.

Pada saluran kemih yang sehat, naiknya infeksi ini biasanya bisa dicegah oleh aliran air kemih yang akan membersihkan organisme dan oleh penutupan ureter di tempat masuknya ke kandung kemih.
Berbagai penyumbatan fisik pada aliran air kemih (misalnya batu ginjal atau pembesaran prostat) atau arus balik air kemih dari kandung kemih ke dalam ureter, akan meningkatkan kemungkinan terjadinya infeksi ginjal.

Infeksi juga bisa dibawa ke ginjal dari bagian tubuh lainnya melalui aliran darah.

Keadaan lainnya yang meningkatkan resiko terjadinya infeksi ginjal adalah:
- kehamilan
- kencing manis
- keadaan-keadaan yang menyebabkan menurunnya sistem kekebalan tubuh untuk melawan infeksi.

GEJALA
Gejala biasanya timbul secara tiba-tiba berupa demam, menggigil, nyeri di punggung bagian bawah, mual dan muntah.

Beberapa penderita menunjukkan gejala infeksi saluran kemih bagian bawah, yaitu sering berkemih dan nyeri ketika berkemih.

Bisa terjadi pembesaran salah satu atau kedua ginjal.
Kadang otot perut berkontraksi kuat.

Bisa terjadi kolik renalis, dimana penderita merasakan nyeri hebat yang disebabkan oleh kejang ureter.
Kejang bisa terjadi karena adanya iritasi akibat infeksi atau karena lewatnya batu ginjal.

Pada anak-anak, gejala infeksi ginjal seringkali sangat ringan dan lebih sulit untuk dikenali.

Pada infeksi menahun (pielonefritis kronis), nyerinya bersifat samar dan demam hilang-timbul atau tidak ditemukan demam sama sekali.
Pielonefritis kronis hanya terjadi pada penderita yang memiliki kelainan utama, seperti penyumbatan saluran kemih, batu ginjal yang besar atau arus balik air kemih dari kandung kemih ke dalam ureter (pada anak kecil).
Pielonefritis kronis pada akhirnya bisa merusak ginjal sehingga ginjal tidak dapat berfungsi sebagaimana mestinya (gagal ginjal).

DIAGNOSA
Diagnosis ditegakkan berdasarkan gejalanya yang khas.

Pemeriksaan yang dilakukan untuk memperkuat diagnosis pielonefritis adalah:
- pemeriksaan air kemih dengan mikroskop
- pembiakan bakteri dalam contoh air kemih untuk menentukan adanya bakteri.

USG dan rontgen bisa membantu menemukan adanya batu ginjal, kelainan struktural atau penyebab penyumbatan air kemih lainnya.

PENGOBATAN
Segera setelah diagnosis ditegakkan, diberikan antibiotik.
Untuk mencegah kekambuhan, pemberian antibiotik bisa diteruskan selama 2 minggu.
4-6 minggu setelah pemberian antibiotik, dilakukan pemeriksaan air kemih ulang untuk memastikan bahwa infeksi telah berhasil diatasi.

Pada penyumbatan, kelainan struktural atau batu, mungkin perlu dilakukan pembedahan.

PENCEGAHAN
Seseorang yang sering mengalami infeksi ginjal atau penderita yang infeksinya kambuh setelah pemakaian antibiotik dihentikan, dianjurkan untuk mengkonsumsi antibiotik dosis rendah setiap hari sebagai tindakan pencegahan.
Lamanya pengobatan pencegahan yang ideal tidak diketahui, tetapi seringkali dihentikan setelah 1 tahun. Jika infeksi kembali kambuh, maka pengobatan ini dilanjutkan sampai batas waktu yang tidak dapat ditentukan.

DM

2009-02-15T16:05:00.000-08:00

Diabetes mellitus (DM) (dari kata Yunani διαβαίνειν, diabaínein, "tembus" atau "pancuran air", dan kata Latin mellitus, "rasa manis") yang umum dikenal sebagai kencing manis adalah penyakit yang ditandai dengan hiperglisemia (peningkatan kadar gula darah) yang terus-menerus dan bervariasi, terutama setelah makan. Sumber lain menyebutkan bahwa yang dimaksud dengan diabetes mellitus adalah keadaan hiperglikemia kronik disertai berbagai kelainan metabolik akibat gangguan hormonal, yang menimbulkan berbagai komplikasi kronik pada mata, ginjal, dan pembuluh darah, disertai lesi pada membran basalis dalam pemeriksaan dengan mikroskop elektron.^[2]

Semua jenis diabetes mellitus memiliki gejala yang mirip dan komplikasi pada tingkat lanjut. Hiperglisemia sendiri dapat menyebabkan dehidrasi dan ketoasidosis. Komplikasi jangka lama termasuk penyakit kardiovaskular (risiko ganda), kegagalan kronis ginjal (penyebab utama dialisis), kerusakan retina yang dapat menyebabkan kebutaan, serta kerusakan saraf yang dapat menyebabkan impotensi dan gangren dengan risiko amputasi. Komplikasi yang lebih serius lebih umum bila kontrol kadar gula darah buruk.

Penyebab

Pembentukan diabetes yang penting adalah dikarenakan kurangnya produksi insulin (diabetes mellitus tipe 1, yang pertama dikenal), atau kurang sensitifnya jaringan tubuh terhadap insulin (diabetes mellitus tipe 2, bentuk yang lebih umum). Selain itu, terdapat jenis diabetes mellitus yang juga disebabkan oleh resistansi insulin yang terjadi pada wanita hamil. Tipe 1 membutuhkan penyuntikan insulin, sedangkan tipe 2 diatasi dengan pengobatan oral dan hanya membutuhkan insulin bila obatnya tidak efektif. Diabetes mellitus pada kehamilan umumnya sembuh dengan sendirinya setelah persalinan.

Pemahaman dan partisipasi pasien sangat penting karena tingkat glukosa darah berubah terus, karena kesuksesan menjaga gula darah dalam batasan normal dapat mencegah terjadinya komplikasi diabetes. Faktor lainnya yang dapat mengurangi komplikasi adalah: berhenti merokok, mengoptimalkan kadar kolesterol, menjaga berat tubuh yang stabil, mengontrol tekanan darah tinggi, dan melakukan olah raga teratur.

Tabel: Kadar glukosa darah sewaktu dan puasa dengan metode enzimatik sebagai patokan penyaring dan diagnosis DM (mg/dl).^[2]	Bukan DM	Belum pasti DM	DM
Kadar glukosa darah sewaktu:
Plasma vena	<110	110 - 199	>200
Darah kapiler	<90	90 - 199	>200
Kadar glukosa darah puasa:
Plasma vena	<110	110 - 125	>126
Darah kapiler	<90	90 - 109	>110

[sunting] Jenis

Organisasi Kesehatan Dunia (WHO) mengakui tiga bentuk diabetes mellitus, yaitu tipe 1, tipe 2, dan diabetes gestasional (terjadi selama kehamilan) ^[3].

[sunting] Diabetes mellitus tipe 1

Diabetes mellitus tipe 1 — dulu disebut insulin-dependent diabetes (IDDM, "diabetes yang bergantung pada insulin"), atau diabetes anak-anak, dicirikan dengan hilangnya sel beta penghasil insulin pada pulau-pulau Langerhans pankreas sehingga terjadi kekurangan insulin pada tubuh. Diabetes tipe ini dapat diderita oleh anak-anak maupun orang dewasa.

Sampai saat ini diabetes tipe 1 tidak dapat dicegah. Diet dan olah raga tidak bisa menyembuhkan ataupun mencegah diabetes tipe 1. Kebanyakan penderita diabetes tipe 1 memiliki kesehatan dan berat badan yang baik saat penyakit ini mulai dideritanya. Selain itu, sensitivitas maupun respons tubuh terhadap insulin umumnya normal pada penderita diabetes tipe ini, terutama pada tahap awal.

Penyebab terbanyak dari kehilangan sel beta pada diabetes tipe 1 adalah kesalahan reaksi autoimunitas yang menghancurkan sel beta pankreas. Reaksi autoimunitas tersebut dapat dipicu oleh adanya infeksi pada tubuh.

Saat ini, diabetes tipe 1 hanya dapat diobati dengan menggunakan insulin, dengan pengawasan yang teliti terhadap tingkat glukosa darah melalui alat monitor pengujian darah. Pengobatan dasar diabetes tipe 1, bahkan untuk tahap paling awal sekalipun, adalah penggantian insulin. Tanpa insulin, ketosis dan diabetic ketoacidosis bisa menyebabkan koma bahkan bisa mengakibatkan kematian. Penekanan juga diberikan pada penyesuaian gaya hidup (diet dan olahraga). Terlepas dari pemberian injeksi pada umumnya, juga dimungkinkan pemberian insulin melalui pump, yang memungkinkan untuk pemberian masukan insulin 24 jam sehari pada tingkat dosis yang telah ditentukan, juga dimungkinkan pemberian dosis (a bolus) dari insulin yang dibutuhkan pada saat makan. Serta dimungkinkan juga untuk pemberian masukan insulin melalui "inhaled powder".

Perawatan diabetes tipe 1 harus berlanjut terus. Perawatan tidak akan mempengaruhi aktivitas-aktivitas normal apabila kesadaran yang cukup, perawatan yang tepat, dan kedisiplinan dalam pemeriksaan dan pengobatan dijalankan. Tingkat Glukosa rata-rata untuk pasien diabetes tipe 1 harus sedekat mungkin ke angka normal (80-120 mg/dl, 4-6 mmol/l). Beberapa dokter menyarankan sampai ke 140-150 mg/dl (7-7.5 mmol/l) untuk mereka yang bermasalah dengan angka yang lebih rendah. seperti "frequent hypoglycemic events". Angka di atas 200 mg/dl (10 mmol/l) seringkali diikuti dengan rasa tidak nyaman dan buang air kecil yang terlalu sering sehingga menyebabkan dehidrasi. Angka di atas 300 mg/dl (15 mmol/l) biasanya membutuhkan perawatan secepatnya dan dapat mengarah ke ketoasidosis. Tingkat glukosa darah yang rendah, yang disebut hypoglycemia, dapat menyebabkan kejang atau seringnya kehilangan kesadaran.

[sunting] Diabetes mellitus tipe 2

Diabetes mellitus tipe 2 — dulu disebut non-insulin-dependent diabetes mellitus (NIDDM, "diabetes yang tidak bergantung pada insulin") — terjadi karena kombinasi dari "kecacatan dalam produksi insulin" dan "resistensi terhadap insulin" atau "berkurangnya sensitifitas terhadap insulin"(adanya defek respon jaringan terhadap insulin)yang melibatkan reseptor insulin di membran sel. Pada tahap awal abnormalitas yang paling utama adalah berkurangnya sensitifitas terhadap insulin, yang ditandai dengan meningkatnya kadar insulin di dalam darah. Pada tahap ini, hiperglikemia dapat diatas dengan berbagai cara dan Obat Anti Diabetes yang dapat meningkatkan sensitifitas terhadap insulin atau mengurangi produksi glukosa dari hepar, namun semakin parah penyakit, sekresi insulinpun semakin berkurang, dan terapi dengan insulin kadang dibutuhkan. Ada beberapa teori yang menyebutkan penyebab pasti dan mekanisme terjadinya resistensi ini, namun obesitas sentral (fat concentrated around the waist in relation to abdominal organs, not it seems, subcutaneous fat) diketahui sebagai faktor predisposisi terjadinya resistensi terhadap insulin, mungkin dalam kaitan dengan pengeluaran dari adipokines ( nya suatu kelompok hormon) itu merusak toleransi glukosa. abdominal gemuk Adalah terutama aktip hormonally. Kegendutan ditemukan di kira-kira 90% dari pasien dunia dikembangkan mendiagnose dengan jenis 2 kencing manis. Lain faktor boleh meliputi mengeram dan sejarah keluarga, walaupun di dekade yang ter]akhir [itu] telah terus meningkat mulai untuk mempengaruhi anak remaja dan anak-anak.

Diabetes tipe 2 boleh pergi tak ketahuan bertahun-tahun dalam suatu pasien [sebelum/di depan] hasil diagnosa [sebagai/ketika] gejala yang kelihatan adalah secara khas lembut atau yang tidak ada,, tanpa ketoacidotic, dan dapat sporadis.. Bagaimanapun, kesulitan yang menjengkelkan dapat diakibatkan oleh jenis tak ketahuan 2 kencing manis, termasuk kegagalan yang berkenaan dengan ginjal, penyakit yang vaskuler ( termasuk penyakit nadi/jalan utama serangan jantung), visi merusakkan, dan lain lain

Diabetes Tipe 2 biasanya, awalnya, diobati dengan cara perubahan aktivitas fisik (biasanya peningkatan), diet (umumnya pengurangan asupan karbohidrat), dan lewat pengurangan berat badan. Ini dapat memugar kembali kepekaan hormon insulin, bahkan ketika kerugian berat/beban adalah rendah hati,, sebagai contoh, di sekitar 5 kg ( 10 sampai 15 lb), paling terutama ketika itu ada di deposito abdominal yang gemuk. Langkah yang berikutnya, jika perlu,, perawatan dengan lisan [[ antidiabetic drugs. [Sebagai/Ketika/Sebab] produksi hormon insulin adalah pengobatan pada awalnya tak terhalang, lisan ( sering yang digunakan di kombinasi) kaleng tetap digunakan untuk meningkatkan produksi hormon insulin ( e.g., sulfonylureas) dan mengatur pelepasan/release yang tidak sesuai tentang glukosa oleh hati ( dan menipis pembalasan hormon insulin sampai taraf tertentu ( e.g., metformin), dan pada hakekatnya menipis pembalasan hormon insulin ( e.g., thiazolidinediones). Jika ini gagal, ilmu pengobatan hormon insulin akan jadilah diperlukan untuk memelihara normal atau dekat tingkatan glukosa yang normal. Suatu cara hidup yang tertib tentang cek glukosa darah direkomendasikan dalam banyak kasus, paling terutama sekali dan perlu ketika mengambil kebanyakan pengobatan.

[sunting] Diabetes mellitus gestasional

Kencing manis mellitus gestasional ( gestational kencing manis mellitus, GDM) juga melibatkan suatu kombinasi dari kemampuan reaksi dan pengeluaran hormon insulin yang tidak cukup, menirukan jenis 2 kencing manis di beberapa pengakuan. [Itu] kembang;kan selama kehamilan dan boleh meningkatkan atau menghilang lenyap setelah penyerahan. Sungguhpun mungkin saja penumpang sementara, gestational kencing manis boleh merusakkan kesehatan dari janin atau ibu, dan sekitar 20%–50% dari wanita-wanita dengan kencing manis gestational kembang;kan jenis 2 kencing manis kemudian (dalam) hidup.

Gestational kencing manis mellitus (GDM) terjadi di sekitar 2%–5% dari semua pregnancies. [Itu] adalah temporer dan secara penuh bisa perlakukan tetapi, tidak diperlakukan, boleh menyebabkan permasalahan dengan kehamilan, termasuk macrosomia ( kelahiran yang tinggi menimbang), bentuk cacad hal-hal janin dan penyakit jantung sejak lahir. [Itu] memerlukan pengawasan hati-hati yang medis sepanjang kehamilan.

Fetal/Neonatal resiko yang dihubungkan dengan GDM meliputi keganjilan sejak lahir seperti berhubungan dengan jantung, sistem nerves yang pusat, dan [sebagai/ketika/sebab] bentuk cacad otot. Yang ditingkatkan hormon insulin hal-hal janin boleh menghalangi sindrom kesusahan dan produksi surfactant penyebab hal-hal janin yang berhubung pernapasan. Hyperbilirubinemia boleh diakibatkan oleh pembinasaan sel darah yang merah. Di kasus yang menjengkelkan, perinatal kematian boleh terjadi, paling umum sebagai hasil kelimpahan placental yang lemah/miskin dalam kaitan dengan perusakan/pelemahan yang vaskuler. Induksi/Pelantikan mungkin ditandai dengan dikurangi placental fungsi. Bagian Cesarean mungkin dilakukan jika ditandai kesusahan hal-hal janin atau suatu ditingkatkan resiko dari luka-luka/kerugian dihubungkan dengan macrosomia, seperti bahu dystocia.

[sunting] Gejala

Tiga serangkai yang klasik tentang gejala kencing manis adalah polyuria ( urination yang sering), polydipsia ( dahaga ditingkatkan dan masukan cairan sebagai akibat yang ditingkatkan) dan polyphagia ( selera yang ditingkatkan). Gejala ini boleh kembang;kan sungguh puasa diset dicetak 1, terutama sekali di anak-anak ( bulan atau minggu) tetapi mungkin sulit dipisahkan atau dengan sepenuhnya absen & & mdash; seperti halnya mengembang;kan jauh lebih pelan-pelan & mdash; diset dicetak 2. Diset dicetak 1 [di/ke] sana boleh juga jadilah kerugian berat/beban ( di samping normal atau yang ditingkatkan makan) dan kelelahan yang tidak dapat diperkecil lagi. Gejala ini boleh juga menjelma diset dicetak 2 kencing manis di pasien kencing manis siapa adalah dengan kurang baik dikendalikan. Gejala awalnya berhubungan dengan efek langsung dari kadar gula darah yang tinggi. Jika kadar gula darah sampai diatas 160-180 mg/dL, maka glukosa akan sampai ke air kemih. Jika kadarnya lebih tinggi lagi, ginjal akan membuang air tambahan untuk mengencerkan sejumlah besar glukosa yang hilang. Karena ginjal menghasilkan air kemih dalam jumlah yang berlebihan, maka penderita sering berkemih dalam jumlah yang banyak (poliuri).

Akibat poliuri maka penderita merasakan haus yang berlebihan sehingga banyak minum (polidipsi).

Sejumlah besar kalori hilang ke dalam air kemih, penderita mengalami penurunan berat badan. Untuk mengkompensasikan hal ini penderita seringkali merasakan lapar yang luar biasa sehingga banyak makan (polifagi).

Gejala lainnya adalah pandangan kabur, pusing, mual dan berkurangnya ketahanan selama melakukan olah raga. Penderita diabetes yang kurang terkontrol lebih peka terhadap infeksi.

Karena kekurangan insulin yang berat, maka sebelum menjalani pengobatan penderita diabetes tipe I hampir selalu mengalami penurunan berat badan. Sebagian besar penderita diabetes tipe II tidak mengalami penurunan berat badan.

Pada penderita diabetes tipe I, gejalanya timbul secara tiba-tiba dan bisa berkembang dengan cepat ke dalam suatu keadaan yang disebut dengan ketoasidosis diabetikum. Kadar gula di dalam darah adalah tinggi tetapi karena sebagian besar sel tidak dapat menggunakan gula tanpa insulin, maka sel-sel ini mengambil energi dari sumber yang lain. Sel lemak dipecah dan menghasilkan keton, yang merupakan senyawa kimia beracun yang bisa menyebabkan darah menjadi asam (ketoasidosis). Gejala awal dari ketoasidosis diabetikum adalah rasa haus dan berkemih yang berlebihan, mual, muntah, lelah dan nyeri perut (terutama pada anak-anak). Pernafasan menjadi dalam dan cepat karena tubuh berusaha untuk memperbaiki keasaman darah. Bau nafas penderita tercium seperti bau aseton. Tanpa pengobatan, ketoasidosis diabetikum bisa berkembang menjadi koma, kadang dalam waktu hanya beberapa jam.

Bahkan setelah mulai menjalani terapi insulin, penderita diabetes tipe I bisa mengalami ketoasidosis jika mereka melewatkan satu kali penyuntikan insulin atau mengalami stres akibat infeksi, kecelakann atau penyakit yang serius.

Penderita diabetes tipe II bisa tidak menunjukkan gejala-gejala semala beberapa tahun. Jika kekurangan insulin semakin parah, maka timbullah gejala yang berupa sering berkemih dan sering merasa haus. Jarang terjadi ketoasidosis. Jika kadar gula darah sangat tinggi (sampai lebih dari 1.000 mg/dL, biasanya terjadi akibat stres-misalnya infeksi atau obat-obatan), maka penderita akan mengalami dehidrasi berat, yang bisa menyebabkan kebingungan mental, pusing, kejang dan suatu keadaan yang disebut koma hiperglikemik-hiperosmolar non-ketotik.

Gejala awalnya berhubungan dengan efek langsung dari kadar gula darah yang tinggi. Jika kadar gula darah sampai diatas 160-180 mg/dL, maka glukosa akan sampai ke air kemih. Jika kadarnya lebih tinggi lagi, ginjal akan membuang air tambahan untuk mengencerkan sejumlah besar glukosa yang hilang. Karena ginjal menghasilkan air kemih dalam jumlah yang berlebihan, maka penderita sering berkemih dalam jumlah yang banyak (poliuri).

Akibat poliuri maka penderita merasakan haus yang berlebihan sehingga banyak minum (polidipsi).

Gejala lainnya adalah pandangan kabur, pusing, mual dan berkurangnya ketahanan selama melakukan olah raga. Penderita diabetes yang kurang terkontrol lebih peka terhadap infeksi.

[sunting] Diabetes dan puasa

Pasien yang cukup terkendali dengan pengaturan makan saja tidak mengalami kesulitan kalau berpuasa. Pasien yang cukup terkendali dengan obat dosis tunggal juga tidak mengalami kesulitan untuk berpuasa. Obat diberikan pada saat berbuka puasa. Untuk yang terkendali dengan obat hipoglikemik oral (OHO) dosis tinggi, obat diberikan dengan dosis sebelum berbuka lebih besar daripada dosis sahur. Untuk yang memakai insulin, dipakai insulin jangka menengah yang diberikan saat berbuka saja. Sedangkan pasien yang harus menggunakan insulin (DMTI) dosis multipel, dianjurkan untuk tidak berpuasa dalam bulan Ramadhan.^[2]