how to generate 2d barcode in c# .net Management of the Acutely Comatose Patient in Microsoft Office

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Management of the Acutely Comatose Patient
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Seriously impaired states of consciousness, regardless of their cause, are often fatal not only because they represent an advanced stage of many diseases but also because they add their own particular burdens to the primary disease The physician s main objective, of course, is to nd the cause of the coma and to treat it appropriately It often happens, however, that the disease process is one for which there is no speci c therapy; or, as in hypoxia or hypoglycemia, the acute, irreversible effects have already occurred
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Table 17-3 Important points in the differential diagnosis of the common causes of coma
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IMPORTANT LABORATORY SPECIFIC DISORDER IMPORTANT CLINICAL FINDINGS FINDINGS REMARKS
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GENERAL GROUP
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Coma with focal or lateralizing signs Cerebral hemorrhage Hemiplegia, hypertension, cyclic breathing, speci c ocular signs (See Chaps 14 and 33) CT scan
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Basilar artery occlusion (thrombotic or embolic)
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Normal early CT; MRI shows cerebellar and brainstem or thalamic infarction, normal CSF CT and MRI show massive edema of hemisphere CT scan; CSF xanthochromic with relatively low protein
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Sudden onset, often with headache, vomiting; history of chronic hypertension; late pupillary enlargement Onset subacute (thrombosis), or sudden (rostral basilar embolism)
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318 Massive infarction and edema in carotid territory Subdural hematoma Trauma Brain abscess Hypertensive encephalopathy; eclampsia Thrombotic thrombocytopenic purpura (TTP) Meningitis and encephalitis Neurologic signs depending on location Blood pressure 210/110 (lower in eclampsia and in children), headache, seizures, hypertensive retinal changes Petechiae, seizures shifting focal signs Stiff neck, Kernig sign, fever, headache Stertorous breathing, hypertension, stiff neck, Kernig sign Subarachnoid hemorrhage
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Extensor posturing and bilateral Babinski signs; early loss of oculocephalic responses; ocular bobbing Hemiplegia, unilateral unresponsive or enlarged pupil Slow or cyclic respiration, rising blood pressure, hemiparesis, unilateral enlarged pupil Signs of cranial and facial injury
CT and MRI show brain contusions and other injuries CT scan and MRI CT ; CSF pressure elevated
Coma preceded by drowsiness for several days after stroke Signs or history of trauma, headache, confusion, progressive drowsiness Unstable blood pressure, associated systemic injuries Systemic infection or neurosurgical procedure, fever Acute or subacute evolution, use of aminophylline or catecholamine medications Multiple small cortical infarctions; thrombocytopenia CT scan ; pleocytosis, increased protein, low glucose in CSF CT scan may show blood and aneurysm; bloody or xanthochromic CSF under increased pressure Similar to fat embolism; multifocal microvasculopathy Subacute or acute onset
Coma without focal or lateralizing signs, with signs of meningeal irritation
Sudden onset with severe headache
Coma without focal neurologic signs or meningeal irritation; CT scan and CSF normal Sedative intoxication Hypothermia, hypotension Drug in urine and blood; EEG often shows fast activity Opioid intoxication Carbon monoxide intoxication Global ischemia anoxia Carboxyhemoglobin CSF normal; EEG may be isoelectric or show high-voltage delta Low blood and CSF glucose Slow respiration, cyanosis, constricted pupils Cherry-red skin Rigidity, decerebrate postures, fever, seizures, myoclonus
Alcohol intoxication Hypothermia, hypotension, ushed skin, alcohol breath Elevated blood alcohol
May be combined with head injury, infection, or hepatic failure
Hypoglycemia Same as in anoxia
Diabetic coma Signs of extracellular uid de cit, hyperventilation with Kussmaul respiration, fruity breath
History of intake of drug; suicide attempt Administration of naloxone causes awakening and withdrawal signs Pallidal necrosis Abrupt onset following cardiopulmonary arrest; damage permanent if anoxia exceeds 3 5 min Characteristic slow evolution through stages of nervousness, hunger, sweating, ushed face; then pallor, shallow respirations and seizures History of polyuria, polydipsia, weight loss, or diabetes
Uremia
Progressive apathy, confusion, and asterixis precede coma
319 Hepatic coma Hypercapnia Papilledema, diffuse myoclonus, asterixis Severe infections (septic shock); heat stroke Seizures Extreme hyperthermia, rapid respiration Episodic disturbance of behavior or convulsive movements
Hypertension; sallow, dry skin, uriniferous breath, twitchconvulsive syndrome Jaundice, ascites, and other signs of portal hypertension; asterixis
Glycosuria, hyperglycemia, acidosis; reduced serum bicarbonate; ketonemia and ketonuria, or hyperosmolarity Protein and casts in urine; elevated BUN and serum creatinine; anemia, acidosis, hypocalcemia Elevated blood NH3 levels; CSF yellow (bilirubin) with normal or slightly elevated protein
Increased CSF pressure; PCO2 may exceed 75 mmHg; EEG theta and delta activity Vary according to cause Characteristic EEG changes
Onset over a few days or after paracentesis or hemorrhage from varices; confusion, stupor, asterixis, and characteristic EEG changes precede coma Advanced pulmonary disease; profound coma and brain damage uncommon Evidence of a speci c infection or exposure to extreme heat History of previous attacks
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