Diagnosis of MELAS
MELAS Diagnosis: Book Excerpts
Diagnostic Tests for MELAS: Online Medical Books
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ACIDOSIS (DECREASED PH):
Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- What is the blood glucose and serum acetone level? If these are increased, consider diabetic acidosis. If these are normal, consider other causes of acidosis.
- What is the bicarbonate level? An increased bicarbonate level points to respiratory acidosis, whereas a decreased bicarbonate level points to renal disease, diarrhea, and the use of certain diuretics.
DIAGNOSTIC WORKUP
This should include a CBC, chemistry panel, electrolytes, arterial blood gas analysis, serum and urine ketones, lactic acid, pulmonary function tests, EKG, and consultation with a pulmonologist or nephrologist.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
LACTIC DEHYDROGENASE ELEVATION:
Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- What is the level of
creatine phosphokinase isoenzyme containing M and B subunits (MB-CPK)
? An elevated MB-CPK combined with elevated LDH is most likely due to a myocardial infarction, although myocarditis and pericarditis can produce a similar picture.
- What is the AST level? If the MB-CPK or CPK are not also increased, an elevation of both the LDH and AST would point to liver disease.
- What are the serum and urine creatine levels? If these are elevated, muscle disease must be considered likely.
- What does the lung scan show? If positive,
a lung scan
separates pulmonary infarction from the other conditions in this group.
DIAGNOSTIC WORKUP
The diagnostic workup should include a CBC, urinalysis, chemistry panel, sedimentation rate, ANA, urine and serum creatine, urine myoglobin, serial EKGs, blood gas analysis, LDH isoenzymes, chest x-ray, lung scan, EMG, and cardiology and neurology consults. A liver scan, CT scan of the abdomen and liver, and muscle biopsy may be necessary.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
ACIDOSIS (DECREASED PH):
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The laboratory will be of greatest assistance in determining the cause of acidosis. An elevated blood sugar and serum acetone level will help diagnose diabetic acidosis. An elevated blood urea nitrogen (BUN) would point to uremia acidosis. Arterial blood gases may show an increased CO2, isolating pulmonary emphysema as the cause.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
ASPARTATE AMINOTRANSFERASE, ALANINE AMINOTRANSFERASE, AND LACTIC DEHYDROGENASE ELEVATION:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Obviously, the first condition to rule out is myocardial infarction. This is done by ordering serial MB-CPKs (MB isoenzyme of creatine phosphokinase) and ECGs. Serum cardiac troponin levels may also be helpful. Next, determine if the patient is on heparin, because this may elevate the alanine aminotransferase (ALT) level. Various muscle diseases (dermatomyositis, muscular dystrophy, muscle trauma, etc.) may be excluded by ordering CPK enzymes also, particularly the MM (MM isoenzyme of creatine phosphokinase) fraction. Liver disease can be revealed through by a liver profile, CT scan of the abdomen, and gallbladder ultrasonography.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
Stroke:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Characteristics of the stroke. What is the duration of the deficit? Is the problem acute and lasting several hours? Impaired consciousness can occur in all types of stroke. More specific symptom may help localize the area of stroke:
1. Carotid circulation: symptoms of hemiplegia, hemianesthesia, aphasia, visual field defects, and loss of spatial function; occasionally, seizures, headache, amnesia, and confusion.
2. Vertebrobasilar circulation: symptoms of diplopia, vertigo, ataxia, facial paresis, Horner’s syndrome, dysphagia, dysarthria, quadraparesis
(a component of bilateral arms or legs), and crossed sensory symptoms (ipsilateral face and contralateral body). Cerebellar lesions often display headache, nausea or vomiting, and ataxia.
B. Past history. A history of trauma, migraine, vasculitis, seizure, and hypoglycemia could produce a condition that can mimic stroke. Fever or infection may suggest abscess. A prior history of stroke or TIA often precedes the presentation of a new stroke. A history of valvular heart disease, atrial fibrillation, or MI is relevant.
C. Risk factors. Patients need to be assessed for hypertension, cardiac disease (specifically atrial fibrillation), smoking, diabetes mellitus, hypercoagulable states, and hormonal therapy.
D. Hospitalization. This may be necessary for patients with transient or ongoing ischemic deficits. TIAs can herald a high-grade carotid stenosis or occult left atrial thrombus.
Physical examination (PE)
A. General examination. This should include vital signs (notably blood pressure), Mini-Mental Status Examination, and an examination of the eyes, including funduscopic. A screening neurologic examination of cranial nerves, coordination, muscle strength, sensation, deep tendon, reflexes, and gait is recommended.
B. Additional PE. Evaluate the heart (arrhythmia, mitral stenosis) and vascular system (carotid bruits), and palpate the scalp and neck (trauma and migraine) and superficial temporal arteries (arteritis).
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Stroke Syndromes:
Differential Overview
(Field Guide to Bedside Diagnosis)
TIA/Stroke
❑ Middle cerebral artery stroke
❑ Anterior cerebral artery stroke
❑ Posterior cerebral artery stroke
❑ Watershed stroke
❑ Thalamic lacune
❑ Vertebrobasilar ischemia
❑ Pontine lacune
❑ Pontine stroke
❑ Midbrain stroke
❑ Pure motor hemiplegia
❑ Ataxic hemiparesis
❑ Lateral medullary stroke
❑ Temporal lobe stroke
Hemorrhage
❑ Subarachnoid hemorrhage
❑ Cerebellar hemorrhage
❑ Thalamic hemorrhage
❑ Pontine hemorrhage
❑ Putaminal hemorrhage
Diagnostic Approach
Brain ischemia leading to stroke may be due to embolism from carotid or cardiac sources, systemic hypoperfusion, or in situ thrombosis. Embolic strokes occur suddenly with maximal focal deficits at the onset. Rapid improvement favors an embolic TIA. Thrombosis symptoms fluctuate in a stepwise pattern. Intracerebral hemorrhage progresses gradually over minutes to hours. Aneurysmal subarachnoid hemorrhage occurs in an instant, and focal brain dysfunction is usually absent. Strokelike symptoms due to migraine are recognized by a headache, epiphenomena such as anorexia/nausea and photophobia, and occurrence in younger patients.
A TIA proceeds to stroke in 10% to 40%. Risk is especially high in “crescendo TIA,” which is usually caused by an ulcerated carotid plaque. Amaurosis fugax (“a shade coming down” or transient monocular loss of vision) is a classic presentation. Amaurosis fugax, an anterior circulation event, should be distinguished from transient hemianopsia, a posterior circulation event. An asymptomatic carotid bruit is an imperfect indicator of carotid stenosis and subsequent stroke risk, with an annual risk of an ipsilateral stroke not preceded by a TIA of 1% to 3% per year.
Examination of the optic fundus may reveal a cholesterol crystal, white platelet-fibrin or red clot emboli. Subhyaloid hemorrhage often accompanies a subarachnoid or intracerebral hemorrhage. A red patch with a white center (Roth spot) may be seen in bacterial endocarditis. With occlusion of the carotid artery, the iris may appear speckled and the ipsilateral pupil dilated and poorly-reactive.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Stroke:
Diagnosis
(Handbook of Diseases)
Confirmation of stroke is based on symptoms, a history of risk factors, and the results of diagnostic tests.
❑ Computed tomography scan shows evidence of hemorrhagic stroke immediately but may not show evidence of thrombotic infarction for 48 to 72 hours.
❑ Magnetic resonance imaging may help identify ischemic or infarcted areas and cerebral swelling.
UNDER STUDY: Positron emission tomography can quantify cerebral blood flow. Single-photon emission tomography, computed tomography perfusion, and magnetic resonance perfusion techniques report relative blood flow and are research tools.
❑ Ophthalmoscopy may show signs of hypertension and atherosclerotic changes in retinal arteries.
❑ Angiography outlines blood vessels and pinpoints atherosclerotic plaques, vessel occlusion, or the rupture site.
❑ EEG helps to localize the damaged area.
Other baseline laboratory studies include urinalysis, coagulation studies, complete blood cell count, serum osmolality, and electrolyte, glucose, triglyceride, creatinine, and blood urea nitrogen levels.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
ACIDOSIS (DECREASED pH):
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The laboratory will be of greatest assistance in determining the cause
of acidosis. An elevated blood sugar and serum acetone level will help
diagnose diabetic acidosis. An elevated blood urea nitrogen (BUN) level
would point to uremia acidosis. Arterial blood gases may show an increased
CO2, isolating pulmonary emphysema as the cause.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
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