BIOCHEMICAL INVESTIGATION OF COMA - Copy.ppt

BIOCHEMICAL INVESTIGATION OF COMA DR GHAZALI SM MB, Ch.B, FMCPath Clinical Pathologist/Metabolic Physician INTRODUCTION • Coma = Unarousable unresponsiveness • Often occur as medical/surgical emergencies • Causes affect both cerebral hemispheres OR the ascending Reticular Activating System (ARAS)...

BIOCHEMICAL INVESTIGATION OF COMA DR GHAZALI SM MB, Ch.B, FMCPath Clinical Pathologist/Metabolic Physician INTRODUCTION • Coma = Unarousable unresponsiveness • Often occur as medical/surgical emergencies • Causes affect both cerebral hemispheres OR the ascending Reticular Activating System (ARAS) • Often requires prompt intervention to save life and restore/preserve brain function • Clinical assessment & management proceed simultaneously Causes of Coma Supratentoral Infratentoral Metabolic Diffuse This lecture is concerned with Comas resulting from Metabolic emergencies and can be referred to as Metabolic Comas • • • • AETIOLOGY Classified as Structural and nonStructural. Most frequent causes easily remembered using the mnemonic TIPPS on the vowels as follows • AEIOUTIPPSS (A=Alcohol, E=epilepsy, I=insulin, O=opiates, U=urea, T=trauma, I=infection, P=poisoning, P=psychogenic, S=shock, stroke PATHOPYSIOLOGY • Bilateral diffuse hemispheric injuries and focal lesions within the upper brainstem damaging the ARAS may reduce alertness (Coma) • Large unilateral lesions exerting pressure on the other hemisphere may also cause coma otherwise it will only diminish arousal • Metabolic diseases, Toxins and drugs affecting the CNS also lead to coma CLINICAL ASSESSMENT • Most cases are due to trauma, CVD, infections, intoxications, and metabolic derangements • Trauma and CVDs complicated by metabolic derangements preceding or following the event • History (when available) & physical findings often give a clue to the causes and occasionally complications • Radiodiagnostic modalities (CT-Scan, MRI) are used in elucidating intracranial structural abnormalties BIOCHEMICAL INVESTIGATIONS Required to rule out metabolic, endocrine and toxicologic causes/complications of coma Metabolic Causes • Hyper/hypoglycaemia • DKA • Addison’s disease • Hypoxia • Hypercapnia • Hepatic Encephalopathy BIOCHEMICAL INVESTIGATIONS Metabolic Causes… • Hyper/hyponatraemia • Hypercalcaemia • Uraemia • Hypothyroidism Toxic Encephalopathy ( Toxins, Poisons, drugs) • Wernicke’s Encephalopathy You want to confirm or r/o the presence of any/some of these in a comatose patient BIOCHEMICAL INVESTIGATIONS Warning signs may be found on GPE • Severe dehydration, acidotic breathing & acetone breath suggests DKA • Bullous lesions xterise barbiturate poisoning • Jaundice could indicate liver disease • A cherry red color, of the lips and mucous membranes, suggests CO poisoning • Needle tracks suggest i/v drug abuse BIOCHEMICAL INVESTIGATIONS The sequence of ordering tests depend on history and examination findings. They include • Serum glucose, E,U & Creatinine (in all cases of coma) • Ca++, Mg++ PO43• Serum Alcohol level • Liver function tests • Arterial blood gases, carboxyhemoglobin level BIOCHEMICAL INVESTIGATIONS • Urinalysis +/- Urine toxicologic studies, myoglobin and Porphobilinogen (rapid dip-stick) • Urinary electrolytes may be useful in suspected addisonian crisis (acute adrenal failure) • Thyroid Function tests • Drug Screening (ethanol, opiates, acetaminophen, salicylates, benzodiazepin, amphetamine, barbiturates…et Cetera) • Carboxyhemoglobin in Suspected CO poisoning METABOLIC COMAS • A cardinal feature is the absence of lateralizing signs • Except in ↑/↓glycaemia, neurological deficits are bilaterally symmetrical in metabolic comas • Tremor, asterixis, & multifocal myoclonus, strongly suggest metabolic coma (organ failure) Urinalysis & Basic Metabolic Profile • Offers rapid, semi-quantitative assays for glucose, ketone, bilirubin, pH, S.G, RBC,... • Capillary blood glucose rapidly estimated from finger prick blood(using a glucometer) • A pulse oximeter to estimate arterial oxygen tension • i-STAT may be used on venous blood/plasma Urinalysis &/ Basic Met. Profile • Moderate to Severe glucosuria with ketonuria suggests (DKA)/hyperglycemic coma • Bed-side pulse oximetry reveals presence/absence of hypoxia • ABG required to confirm hypercapnia • Always correct Calcium if needed. Thyroid function • TSH high in myxoedema coma with • Low FreeT3, FreeT4 or both • Free T4 alone is better than Free T3 alone • High TSH with low FreeT3/T4 • Medical history and exam reveal suggestive features Addison's disease & AKA Hyponatremia, hyperkalemia & mild non anion gap metabolic acidosis •ACTH, cortisol, (low cortisol with high ACTH) Assay cortisol & aldosterone after ACTH injection. •Acetone breath, hypoglycaemia, high AG acidosis suggests alcohol, normal pH from vomitting may mask the acidemia Drug abuse • History & exam findings raise suspicion • specific drug metabolites may be assayed using HPLC, GLC (if available) • Naloxone may be given when opiates are suspected • Stabilise patient and refer for better assesment and further management Conclusion Individual causes of coma are inexhaustible, the ones we list only represent the most commonly encountered cases. Evaluation and treatment are targeted towards the most life threatening causes in order to preserve life and restore health THANK YOU ALL FOR LISTENING ABBREVIATIONS • ABG: Arterial Blood gases • ARAS: Ascending Reticular Activating System • CVD: Cerebrovascular diseases • CO: Carbon Monoxide • High Performance Liquid Chromatography • Gas Liquid Chromatography