Lectures

• General causes of coma are: Structural, metabolic, drugs, cardiovascular, respiratory, sepsis, neurological, alcohol and toxic exposure
• Within structural causes of coma theres: CVAs, TBIs and tumors
• A patient is never "just drunk" so don't half ass assessments in these cases
• Bowel obstructions can cause the release of endotoxins in the body which causes vasodilation and drops BP
• In structural assessments, neuro findings are asymmetrical such as Pupils unequal
• In toxic/metabolic findings, assessments are symmetrical and and have a gradual onset; ensure to ask changes in their behaviour
• Hypoglycemia is wet while hyperglycemia is dry
• Within metabolic assessments: there's diabetes(hyper/hypoglycemia), adrenal crisis, kidney and liver failure and electrolyte imbalance
• Hyperglycemics are in a state called diuretic osmosis; increased urination due to the prescence of excess glucose in filtrate(this increases osmotic pressure and forces water and K+ to be excreted).
• Hyperglycemics piss a lot and drink a lot
• Renal failure psychosis: toxins from the kidneys due to lack of filtration cause psychosis
• There's preceding symptoms in electrolyte imbalances before loss of LOAs; these are: muscle cramps and arrhythmias
• Alcohol is very good at mimicking and masking other drugs
• Barbiturates often mixed with narcotics and have a very strong sedative effect that leaves Pts in a rigid position
• Sepsis causes: meningitis, encephalitis, nuchal rigidity(stiff neck) and headache with very high fever
• TIAs are a prelude to a stroke and are often called mini strokes
• Alcohol withdrawal can cause seizures
• Toxicity findings include: CO(fossil fuels, gas, propane) and Cyanide gas
• Cyanide gas is released from in fires or burning objects
• Toxicity relates to anything that causes hypoxia
• Blink test: touching a Pts eyelashes lightly to see if there's a reflex; used to check if someone is truly unconscious
• Diagnostic tests are ETCO2, SPO2, temperature, ECGs and BGL
• LOC terms are: drowsiness, stupor and coma
• In drowsiness, Pt is asleep but easily stirred by verbal
• The goals regarding an unresponsive PT is to: support PT's vital functions, prevent further deterioration, consider/treat reversible causes and then rapid transport
• Cold and dry skin may indicate sedative or alcohol abuse
• BLS general principles of managing the comatose Pt: maintain airway/breathing, monitor circulation, position PT appropriately, consider C-spine, initiate rapid transport, reassess vitals and neurologic every 5 to 10 minutes. In addition, assess for hypoglycemia, establish an IV, establish transport position and priority, protect any paralyzed extremities, provide protection/privacy and remember PT has no muscle tone
• In stupor, a PT does not respond to verbal but pain stimuli
• In coma, PT doesn't respond to any kind of stimuli; GCS 3
• Glucose is the only substance brain cells can use but it can't store it
• Type 1 diabetes is referred to as IDDM(Insulin dependent diabetes mellitus) in which a PT takes insulin injection, has a glucometer and monitors blood sugar levels
• Type 2 diabetes is NIDDM(Non-insulin dependent diabetes mellitus) in which there's an insulin resistance. This is often diet controlled or medicated through Oral hypoglycemic agents(OHA)
• OHA are: Metformin, Glyburide and Gluconorm
• Metformin: decreases glucose production by the liver and increases cell sensitivity to insulin
• Glyburide: a common drug in a class called sulphonylureas and function in long acting increase in insulin production
• Gluconorm: belongs to a class called meglintides and are similar to sulphonylureas but these are short acting and often taken with food
• Hyperglycemia and DKA usually occurs in younger, lean PTs with type 1 Diabetes. Develops over a day or so. S/S: are deep, rapid respirations or Kussmaul's respirations and acetone breath.
• Hyperosmolar hyperglycemic syndrome(HHS) usually occurs in older, obese PTs with type 2 diabetes. It takes days to weeks to develop and often in the elderly due to decreased renal function
• In DKA, blood sugar is high but glucagon is still breaking down stored sugar. EPI and cortisol are released to break down fat and glycogen to sugar which can release byproducts such as acids and ketone bodies.
• DKA is a profound state of hyperglycemia