Metabolic Emergencies Flashcards
2 major causes of hypoglycemia
1) excess endogenous/exogenous insulin or hypoglycemic agents (metformin, TZDs, sulfonlyureas)
2) failure of other organs to produce or mediate glucose metabolism (pancreas, liver)
glucose reference range
~65-110 mg/dl
when does the body usually stim catecholamine release
Glucose 30-50 mg/dL
what are the effects of a catecholamine release
Irritability, hunger (“hangry”), trembling
Diaphoresis
Tachycardia
what glucose level are there neuroglycopenic effects
less than or equal to 30
Neuroglycopenic effects of low glucose
Focal neurologic deficits, headaches, dizziness
Confusion, bizarre behavior, visual disturbances
Hypothermia
Seizure or seizure-like activity
tx of hypoglycemia if IV is not available
IM glucagon
how does IM glucagon work
trigger liver to convert glycogen to glucose (glucagon is typically release by pancreatic alpha cells in response to hypoglycemia)
tx of hypoglycemia with IV access
Glucose
IV D50 (IV dextrose)
Oral glucose gel/tabs
If conscious and responsive with mild
hypoglycemia: OJ, candy, a snack or meal
*what is DKA
Profound deficiency of insulin results in hyperglycemia
Results in hyperglycemia
(has glucose but there is no insulin to put it in the cells)
*MC life threatening condition with DM (typically type I)
DKA
*lack of insulin in DKA leads to…
breakdown of triglycerides/fatty acids for energy with production of ketones
*often initial clinical presentation of Type I DM
DKA
*onset of DKA
rapid (within days of symptom onset)
*symptoms of DKA
Polyuria & polydipsia
Headache
Abdominal pain
Nausea & vomiting
Weakness/lethargy
Kussmaul respiration
Deep, rapid, sighing; aka air hunger
Depressed mental status
Dehydration
*acidosis (fruity breath)DKA labs:
- serum glucose
- ketones
- serum bicarb
- arterial pH
Serum Glucose > 250mg/dl
Ketones
Ketonuria
Serum ketones
Serum Bicarbonate < 15mEq/lL
pH <7.3*DKA Labs: Anion Gap Serum Sodium Serum Phosphate Serum Potassium
Elevated Anion Gap (see next slide)
Serum Sodium – usually low (osmotic hemodilution)
Serum Phosphate – low (hemodilution and diuresis)
Serum Potassium – often normal to elevated
Paradoxical elevation caused by extracellular shift
of potassium resulting in a relative hyperkalemia
what is a normal anion gap, how is it calculated and what is it for
Anion Gap = Serum NA+ – (Serum Cl- + HCO3-)
Normal: ~8 +/- 4 mmol/L
Generally accepted > 12 mmol/L = elevated
causes of increased anion gap and what is it for
MUDPILERS: DKA Methanol Uremia Diabetic/alcoholic/starvation ketosis Paraldehyde Isoniazid/Iron Lactic acidosis Ethylene Glycol Rhabdo, Salicylates
*step 1 tx for DKA
IV Fluids: Normal Saline @ 500-1000 ml/hr
-DO 1st! Why?? –> when give insulin, the glucose
goes into he cells and the water follow and their BP
can tank
-Once orthostatic hypotension resolves (fluid loss due
to polyuria), decrease to 200-500 cc/hr.
*step 2 tx for DKA
Insulin 10 U bolus and then 5 U/hr.
-~1hr post IVF
-Follow blood sugar: expect serum glucose to
decrease at 100/hr
-Lower blood glucose, gradually, to <250
-If inadequate fall in blood glucose, the insulin
and the IVF
*step 3 tx for DKA
Potassium replacement considered
-Pre-labs:
-If urinating and non-peaked T waves; add 20
mEq to IV
-If urinating and flat/depressed T waves or U
waves; add 40 mEq to IV
-If anuric and peaked T waves – await labs to
determine amount
*why do you not want to decrease glucose too quickly in DKA and what should you keep glucose levels at
Too rapid of a correction can lead to sequelae such as cerebral edema
150-250 mg/dL
*onset of HHS
insideous
*what is HHS
adequate insulin, decreased cell response
*HHS is MC in…
Type II DM
*cause of HHS
precipitating event
*labs for HHS
- severely elvated glucose (>600)
- absence of lipolysis/ketogenesis
- low/absent serum/urine ketones
*typical HHS pt
Typically ≥ 60 years old
Chronic care facility or nursing home
Change in diabetic regimen or addition of meds that raise glucose levels
Corticosteroids, thiazides, anticonvulsants,
sympathomimetics
Recent or current infection
Dementia
*is kussumal signs present in DKA, HHS, or both
DKA ONLY
*s/sxs HHS
- N/V-abdominal pain
- sig dehydration
- depressed mental status
- Focal neurologic abnormalities
- NO kussumal signs
*t/f-pH is decreased in HHS
FALSE, pH is normal in HHS!
DKA has low pH
tx for alcholic ketoacidosis
*thiamine 100mg IV or IM –> for neuron function
what is thyroid storm
extreme form of thyrotoxicosis
clinical manifestation of thyroid storm
Fever – may exceed 104°F Tachycardia (Sinus, SVT, Atrial arrhythmias, CHF) Delirium, confusion N&V and diarrhea, abdominal pain Agitation, tremor, generalized weakness
labs for thyroid storms
TSH (low), Free T4 (high)
what should you avoid as tx for someone with thyroid storm
ASA- displaces t4
myxedema coma
severe hypothyroidism
s/sxs of myxedema coma
Hypothermia
Hypoventilation leading to hypoxia and hypercapnia
Hyponatremia
Hypotension
Seizures and abnormal CNS signs may occur including altered mental status.
what med is myxedema coma pts very sensitive to
opiates- a normal dose can kill them
tx for myxedma coma
1) loading dose of 500 micrograms of levothyroxine
2) hydrocortisone 100mg IV bolus followed by 25-50 every 8 hrs
*adrenal insufficiency dx
synthetic ACTH (cosyntropin) stimulation test
