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]
Minggu, 15 Februari 2009
Gangguan Gizi
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
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
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
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
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