Endocrine Emergencies Flashcards
Pt is confused, sweaty, tachycardic with blurry vision and has Type 1 DM, what should be ordered?
Fingerstick glucose
UA/microscopy
Urine pregnancy test
Lab definition of hypoglycemia
<70 mg/dL (some will say <54 to avoid over diagnosing asymptomatic pts)
Causes of hypoglycemia
Delay in eating (esp after taking insulin)
Poor caloric intake (dieting, vomiting)
Increased or unusual physical exertion
Increased physiologic stress (like infection/trauma etc)
Alternations in therapeutic regimen
Accidental excessive dose of exogenous insulin
If using insulin, variable absorption at injection site
Excessive insulin release caused by sulfonylurea (esp in presence of renal insufficiency)
When do you see hypoglycemia more?
Type 1 (over type II or non-diabetics)
Management of asymptomatic hypoglycemia (pt with drug treated DM and glucose <70 mg/dL)
Defensive action-repeat measurement in near future, avoid critical tasks like driving, ingesting carbs and adjusting treatment regimen
Management of symptomatic hypoglycemia but pt is awake
15-20 grams of oral carbohydrate (either 3-5 glucose tablets/ hard candies or 1/2 cup juice/non-diet soda)
Why use 15-20 g carbohydrate to treat hypoglycemia?
B/c it will raise the blood sugar without inducing hyperglycemia!
-can follow it up with a long acting carbohydrate in order to prevent recurrence tho!
Management of severe hypoglycemia with AMS
They are usually unable to safely swallow oral glucose SO
SubQ or IM injection of .5-1.0 mg of glucagon (must be mixed in order to use)
What happens when you give a severely hypoglycemia person glucagon?
The consciousness is recovered in less than 15 min BUT it may be followed by nausea and vomiting! (profuse)
What is a quicker way to treat hypoglycemia?
25 g of 50% glucose (dextrose) IV–1 amp of D50
What must come after you give a patient D50?
Subsequent glucose infusion or if patient’s mental status allows them to eat then give food
When will a pts mental status normalize?
When blood glucose increases into the normal range (for hypoglycemia)
What are classic worrisome sxs that might be seen with hypoglycemia?
Stroke-like sxs with a focal neurological exam (can’t move arm)-should resolve when fix the glucose
Is it ok to just let the pt go after giving them glucose and their mental status gets better?
NO b/c it might reoccur (should observe the pt for some time to check serial blood sugars to figure out cause and to fix the problem)
What must be done if a pts hypoglycemia was due to a sulfonylurea?
ADMIT b/c half life of the drug is so long that condition is almost guaranteed to come back
What is the reason for a metabolic acidosis (ph low and low bicarb) with an anion gap?
MUDPILES
Methanol, uremia, DKA, propylene glycol, iron/isoniazid, lactate, ethanol/ethylene glycol, salicylates/starvation
*low PCO2 if compensating by hyperventilating to blow off CO2
How to calculate anion gap
Na-(Cl+HCO3)
Normal is <10 (elevated is >12?)
What does metabolic acidosis cause related to the abdomen?
Peritoneal signs (so will have abd pain)
What precipitates both DKA and HHS?
Infection!! (UTI or pneumonia)
Trauma/surgery
MI/stroke
Insulin omission (not taking it or not knowing that need it)
What is HHS?
Hyperosmolar hyperglycemic state (hyperglycemic hyperosmolar non-ketotic state)
When is DKA seen more?
Almost always in type 1 DM as a result of insulin insufficiency in the setting of a precipitant
Sxs of DKA
-develop over hours to days Abd pain/n/v Hyperventilation (Kussmaul respirations-fast and deep) Hypotension/shock/dehydration Metabolic acidosis with increased anion gap Elevated glucose Elevated serum ketones Polyuria, polydipsia, weight loss
What can present as DKA?
Can be the presenting sign of diabetics in 1/4 of type 1 diabetics (so don’t exclude diagnosis if history is none)
Glucose and DKA
Generally between 350-500 (but diagnosis is not based on the elevation of glucose)
*in order to have DKA there must be other lab abnormalities
Other labs in DKA
Ketones: urine and serum positive
Potassium: high, low or normal (generally body has a significant K+ deficit)
Sodium: usually low but also falsely lowered
Chloride: low in anion gap
Bicarb: low
BUN/Cr: elevated (dehydration)
Anion gap: elevated
Serum osmolarity: elevated (NOT as much as with HHS)
Potassium management of DKA
Usually elevated at presentation (insulin deficiency and hyperosmolality result in K movement out of cells)
K+ falls precipitously with tx of hyperlgycemia so must watch it closely!! (be prepared to supplement early- bad for heart when drops)
How to correct sodium levels in DKA
For every 100 glucose is above 100, add 2 to Na to correct it
Diagnostics for DKA
Elevated WBC (even if no infection b/c its a stress reaction)
ABG: may have multiple acid base disorders but should be acidosis over all
UA and CXR may show infection
EKG: maybe MI, electrolyte abnormalities or arrhythmias
Head Ct might show stroke
Goals for tx of DKA
Make diagnose and ABCs Restore circulatory volume Correct serum osmolarity Clear serum ketones Correct lytes and anion gap Treat underlying causes Reduce blood glucose
How to treat DKA
ABCs Isotonic saline (.9 normal saline) IV Correct electrolytes (replete K and follow, follow Na, replete phosphate if severe deficit) Control blood glucose Revere acidosis and ketogenesis
How to reverse acidosis and ketogenesis in DKA
Insulin bolus IV (not always tho) or continuous IV insulin infusion
How to manage fluids in DKA
Give IV fluids aggressively
15-20 mL/kg lean body weight per hour (with max of 50 ml/kg in first 4 hrs)–check hydration status, electrolyte levels and urine output after 2-3 hrs to determine how much more
What should be added to the IV fluids with DKA when blood glucose gets to 200-250?
Add dextrose to saline b/c trying to treat the ketogenesis not get normoglycemia (this will be the substrate for the insulin so that won’t need to be making ketones anymore)
Bicarb and DKA?
General rule is that bicarb should not be given in DKA b/c there are lots of complications when trying to raise pH
It might also slow the rate of recovery of ketosis (which we want to do quickly)
Maybe can accelerate ketogenesis too
Complications of bicarb to increase pH
Hypernatremia, hypokalemia, paradoxical CSF acidosis and residual serum alkalosis
What is paradoxical CSF acidosis?
Increased blood bicarb will reduce the hyperventilatory drive which raises the blood pCO2
This causes an increase in uptake of CO2 by cells to cause an intracellular cerebral acidosis!
Then you get your paradoxical fall in cerebral pH leading to neurologic deterioration (cerebral edema and brain damage)
What is the one setting in which to administer bicarb with DKA?
When there is significant hyperkalemia (b/c it will shove the K into cells rather quickly)
(some say to do it when pH <6.9 but who knows)
So therefore what is the mainstay of tx for ketoacidosis?
Fluids and insulin (glucose can enter the cells and the body will immediately discontinue lipolysis as fuel– blood glucose lowers and ketones in blood clear)
What to do if glucose normalizes but still an elevated anion gap?
Continue insulin administration (b/c the presence of insulin will stop the lipolysis_
When do we see HHS?
Mainly type 2 and usually with a precipitant (infections, MI, other stressors)– older nursing home pts
Sxs of HHS
Insidious onset in days to weeks Altered state of consciousness (more likely than in DKA) Weakness (generalized and focal) Polydipsia and polyuria Dehydration
Will the HHS pt have abdominal pain and Kussmaul respirations?
No b/c not acidotis
Pathophysiology of HHS
Hyperglycemia leading to glycosuria and dehydration (hemoconcentration that worsens the hyperglycemia)
Relative insulin deficiency (insufficient to prevent hyperglycemia and glycosuria but sufficient to prevent lipolysis and ketogenesis!!!- why not acidosis)
Lab values of HHS
Glucose>500
Plasma osmolality >320 due to dehydration (often 5-10 liters deficient)
Tx of HHS
Fluid and electrolyte replacement (just like DKA)
Insulin IV (if fluid replacement alone is inadequate to decrease glucose–transition to SQ–transition to home regimen or optimize outpatient therapy)
And treat the underlying problem!
What EKG signs are seen in hyperthyroidism?
Afib with rapid ventricular response (can be ST depression too)
Hyperthyroidism vs thyrotoxicosis vs thyroid storm
Hyperthyroidism: inappropriately elevated thyroid function
Thyrotoxicosis: excessive amt of circulating thyroid hormone (just a lab value)
Thyroid storm: rare and maybe fatal complication seen in untreated or partially treated thyrotoxicosis
Diagnostic criteria for thyroid storm
Based on presence of severe and life-threatening sxs (hyperpyrexia, cardiovascular dysfunction, altered mentation) in a pt with biochemical evidence of hyperthyroidism:
- elevation of free T4 and/or T3
- suppression of TSH
Who will get a thyroid storm?
Pts with long standing untreated/undertreated hyperthyroidism (graves, TMG, solitary toxic adenoma)
BUT often precipitated by acute event like thyroid or non-thyroid surgery, trauma, infection, an acute iodine load or post partum
Presentation of thyroid storm
All normal hyperthyroid sxs PLUS
Hypermetabolism (weight loss/diarrhea)
Excessive adrenergic response
Maybe hyperpyrexia, Afib with possible HF, goiter, exophthalmos, tremor, moist skin, shock, confusion/ agitation/coma
Supportive care used for thyroid storm
ICU admission (ABCs and support) Cooling measures (antipyretics or cooling blankets) Appropriate IV fluid resuscitation Electrolyte replacement Nutritional support
Purpose of thyroid specific therapy for thyroid storm
Prevent thyroid hormone release
Decrease peripheral action of circulating thyroid hormone (reduce HR, support circulation)
Treat precipitating condition
Difference in tx between thyroid storm and uncomplicated thyrotoxicosis
Same options but drugs given in higher doses and more frequently
Medication options for thyroid storm
Beta blocker (propranolol) Thionamides (PTU or methimazole) Iodine solution (KI-iodine or Lugol's solution or super saturated potassium iodide) Glucocorticoids (hydrocortisone) Bile acid sequestrants (cholestyramine)
Why is propranolol used in thyroid storm?
Inhibits type 1 deiodinase (may help to reduce serum t33 levels) and reduce HR
Sequence of tx for thyroid storm
Beta blocker first to control tachycardia!
Then thionamide
1 hr AFTER thionamide, administer iodine solution (must be that time to prevent iodine from being used as substrate for new hormone synthesis)
What does PTU do?
Decrease thyroid hormone synthesis and block conversion of thyroxine (T4) to triiodothyronine (T3)
*lower serum T3 levels for first few days so maybe preferred in storm
What does methimazole do?
Decrease thyroid hormone synthesis (does not inhibit T4-T3 conversion)
When is methimazole preferred over PTU?
Severe but not life threatening hyperthyroidism
-Has longer half life, lower risk of hepatic toxicity and ultimately restores euthyroidism more quickly
What must occur with inpatient on PTU?
Must be transitioned to methimazole before discharge
What are the adjunct txs for thyroid storm?
*given simultaneously
Glucocorticoid to reduce 4-3 conversion, promote vasomotor stability and maybe treat associated relative adrenal insufficiency!
Bile acid sequestrants to decrease enterohepatic recycling of thyroid hormones
How to put together the tx for thyroid storm?
5 Bs: Block synthesis (antithyroid drugs) Block release (iodine) Block conversion Beta-Blocker Block enterohepatic circulation
Treatment of choice when pt allergic to or has contraindication to thionamides or its refractory to meds
Thyroidectomy
What is myxedema coma?
Rare complication of severe hypothyroidism leadign to severe deficiency in thyroid hormone and encephalopathy
Can be the culmination of severe, long standing hypothyroidism (under treated or undiagnosed)
Can be precipitated by event (infection, MI, cold exposure of sedative drugs)
Hallmark features of myxedema coma
Hypothermia
CNS depression/coma
(hypotension, bradycardia, hyponatremia, hypoglycemia and hypoventilation
Who is at highest risk for myxedema coma?
Elderly (especially women)
What is myxedema?
Puffiness of hands and face, thickened nose, swollen lips and enlarged tongue may occur secondary to nonpitting edema with abnormal deposits of mucin in skin and other tissues
What is pretibial myxedema?
Uncommon skin disorder that occurs in autoimmune thyroid disease (mostly graves)
Very important for myxedema coma?
Mortality for 30-40% but when recognized and treated it drops
When should you have a high index of suspicion for myxedema coma?
When clinical manifestations or history of hypothyroidism are accompanied by disturbances of consciousness, hypothermia, hypoventilation and hypotension
Diagnostic studies for myxedema coma
All usually normal unless related to precipitating events
CBC, CMP, CT head, CXR, EKG and ABG
Most common thyroid studies for myxedema coma
Most will have primary hypothyroidism with high TSH and low FT4 (can have normal or low if it is related to hypothalamus or pituitary)
Management of myxedema coma
Well you gotta make the diagnosis ABCs T3 and T4 Glucocorticoids (given until adrenal insufficiency is ruled out) Isotonic fluids Correct lyte problems Rewarming blankets Treat precipitating cause Slow recovery
Thyroid hormones in management of myxedema coma
T4 (IV until can take orally)
T3
Probs best to give both together
What is the problem with T3?
It is the more active form so it can reverse myxedema coma quicker but can also precipitate MI or arrhythmias (so start with lower doses)
What is adrenal insufficiency?
Occurs when lack of cortisol (produced by adrenal glands)
Primary adrenocortical insufficiency
Adrenal gland is damaged/not functioning and it cannot produce glucocorticoids or mineralocorticoids
Addisons
Secondary adrenocortical insufficiency
Involves defect of pituitary gland inhibiting proper release of ACTH (can be isolated or in conjunction with other pituitary hormone deficiences-panhypopituitarism)
Tertiary adrenocortical insufficiency
Suppression of hypothalamic-pituitary-adrenal function
-Mineralocorticoid secretion is basically normal b/c depends on RAAS not ACTH
Most common cause of tertiary adrenocortical insufficiency
Abrupt withdrawal of chronic administration of high doses of glucocorticoids (COPD and chronic prednisone use)
What is an acute adrenal crisis?
Results from acute exacerbation of chronic insufficiency usually caused by sepsis or surgical stress (primary insufficiency)
Can be caused by adrenal hemorrhage, infarction, anticoagulation complications or congenital abnormalities
Presentation of acute adrenal crisis
N/v/d, abd pain, confusion, coma, fever, hyponatremia, hypoglycemia, weight loss
PROFOUND HYPOTENSION
What is Waterhouse Friderichsen syndrome?
Adrenal infarction due to meningococcemia
Think with fever, mental status changes and purpura
Management of acute adrenal crisis
ABCs and IV fluids
Administer hydrocortisone (IV)
Administer mineralocorticoid (Florinef) but not as important as the hydrocortisone
If suspect sepsis, get culture and empirically treat
What might possibly be underlying cause of adrenal crisis?
HIV, metastatic disease, TB or autoimmune adrenalitis
So what to do if suspect an adrenal crisis in any pt?
Treat immediately with hydrocortisone (consider mineralocorticoids)
When to think adrenal crisis
When shock is otherwise unexplained and inadequately responsive to vasopressors and vol replacement
