Endocrine Emergencies Flashcards
Hypoglycemia defined
Glucose < 70 mg/dL
Symptomatic hypoglycemia with levels <50
Risk factors for hypoglycemia in type II diabetes
Age
PMHx of vascular disease
Renal failure
Decreased food intake
Alcohol use
Drug interactions
Non compliance
Hypoglycemia sympathomimetic symptoms
Sweating, tremor, pallor, nausea,
anxiety, palpitations
Hypoglycemia Neuroglycopenia symptoms
Dizziness, psychosis, confusion, coma,
agitation, seizures
Hypoglycemia additional causes
● Insulinoma- Pancreatic islet cell tumor (90% benign)
● Medications/Drugs/Alcohol
● Extrapancreatic neoplasm
● Hepatic disease(depletion of glycogen stores)
● Deficiency of counterregulatory hormones
● Critically ill, stressed infants, hypothermia
● Dumping syndrome
● Artifactual
Hypoglycemia treatment
Standard treatment options
- Oral Glucose
Sugar Water
- D50 (50% dextrose in water) - 50 mL bolus provides 25gm of glucose (500mg/mL)
- D25 (peds)
- D10 (neonates)
- Maintain glucose at > 100 mg/dL
Recheck blood sugar q30 mins
- IV infusion of D10 (10% dextrose in water) or oral to maintain blood sugar
Glucagon 1mg IM/IV
- Stimulates glycogenolysis
- Can raise BS by ↑ 100mg/dL
- Works slower (10-15 minutes)
secondary causes of hypoglycemia if failure to respond to initial therapy
Sepsis, toxin, insulinoma, hepatic failure, adrenal insufficiency
Octreotide (Sandostatin)
- Inhibits insulin secretion
- Helps prevent rebound hypoglycemia in setting of glucose Infusion treatment and persistent symptoms refractory to
sulfonylurea-induced hypoglycemia (As an antidote) - 50-100 mcg SC or IV
Give _____ with glucose in malnourished hypoglycemic patients
thiamine
Diagnosis of DM
- Fasting glucose (100-125 mg/dL)
- Random glucose (>200 mg/dL)
- 2 hour oral glucose tolerance (>200 mg/dL)
- HbA1c of >6.5%
Severe Hyperglycemia (>300 mg/dL) treatment
- Fluids IV
- Insulin -Regular insulin at 0.1- 0.15 units/kg IV or SC (IV better absorption)
Appropriate to initiate Metformin 500 mg qDay - Make sure creatinine is normal
- If modest elevation, inform patient of concern, F/U PCP
Hypoglycemic medications
- Sulfonylurea agents:
- (2nd gen) Glipizide, glimepiride, glyburide
- Stimulate pancreatic insulin secretion
- Cause profound hypoglycemia in OD
- Long duration of action
- Repaglinide (Prandin)
- Stimulates insulin secretion
- Can also cause hypoglycemia
Antihyperglycemic Agents (less likely to cause hypoglycemia in overdose)
Metformin
- Rarely causes lactic acidosis
Less risk of hypoglycemia
GLP-1 agonist
SGLT2 inhibitors
DPP-4 inhibitors
Thiazolidinediones
Diabetic Ketoacidosis Pathophysiology
Defined as cellular starvation due to relative or a
complete lack of insulin:
- Hyperglycemia
- Osmotic diuresis
- Prerenal Azotemia
- Ketone formation
- Wide anion gap metabolic acidosis
Free Fatty acids are converted to Ketones
in the liver → ______
Metabolic Acidosis
Hyperglycemia effects on the body
Glycosuria
Osmotic diuresis
Decreased GFR
Intracellular dehydration
Impaired consciousness
Shock
(Table on slide 20)
Loss of islet cell function in DKA causes what effects on the body?
- Autoimmune destruction → Type I
- Leads to inability of cells to use glucose for fuel, despite
increased levels of intravascular glucose - Breaks down protein and adipose stores
- Increased counterregulatory hormones further leads to
ketonemia and increased hyperglycemia (Osmotic Diuresis)
Precipitants of DKA
Noncompliance with Insulin
Infection
Myocardial Infarction
Pregnancy (IUP)
CVA
Trauma
Hyperthyroidism
Pancreatitis
Any acute stressor
Metabolic acidosis causes compensatory ____
hyperventilation
- Kussmaul breathing
- Acetone leads to fruity breath smell
Avenues of volume loss in DKA
- Osmotic Diuresis
- Vomiting (Acidosis)
- Loss of potassium
- Leads to further hyperglycemia
- Poor absorption of SC Insulin
- Leads to poor Hemodynamics
Diabetic Ketoacidosis diagnosis
- Glucose >250 mg/dL
- Anion gap > 10 mEq/L
- Bicarbonate < 15 mEq/L
- pH < 7.3
Initial Goals and goal labs in treating DKA
- 1st - Volume replacement
- 2nd- Potassium Correction
- 3rd- Insulin Therapy
Goal labs:
- Glucose <200
- Lower Glucose 75 mg/dL/ hr
- >18 mEq/L
- pH >7.3
Fluids / Bicarbonate in DKA - treatment
- Initial fluid resuscitation for hypovolemia
- Replace electrolytes
- Insulin drip
- Sodium bicarbonate is rarely indicated
- As glucose normalizes, start Dextrose
What is Pseudohyponatremia
Sodium is artifactually decreased 1.6 mEq/L for every
100 mg/dL increase in glucose over 100
- After initial bolus, if eunatremic, then switch to 0.45% saline
Complications of DKA Treatment
Hypoglycemia- due to excess insulin
Begin giving glucose when glucose = 200-250
Hypokalemia- from insulin, bicarbonate, hydration
CSF acidosis- bicarbonate
Cerebral edema- Neurologic change
How to treat neurologic changes in DKA
50% of fatalities in DKA
Possibly over-hydration, hypoxemia,
Bicarbonate, rapid osmotic changes
Tx- Mannitol, restrict fluid, intubation
Alcoholic Ketoacidosis
- Binge drinking with heavy
alcohol, - decreased food intake
- starvation ketosis
- EtOH metabolism inhibits
gluconeogenesis - Depletes Glycogen stores
- Abdominal pain, nausea,
vomiting, dehydration,
disorientation
Treatment for alcoholic ketoacidosis
- D5 Normal Saline
- Thiamine
- Electrolyte correction
Anion Gap Metabolic Acidosis causes (MUDPILES)
Methanol/ Metformin
Uremia
Diabetic Ketoacidosis, Alcoholic Ketoacidosis
Paraldehyde
Iron, Isoniazid, Inhalants
Lactic Acidosis
Ethylene Glycol (AntiFreeze)
Salicylates
Hyperosmolar Hyperglycemic Syndrome is similar to DKA except:
- Triggered with concurrent
inflammatory condition - Hyperosmolar, No ketoacidosis
- Glucose usually higher(>1000)
Precipitating factors for HHS
Infection, especially pneumonia
Myocardial infarction
CVA
GI bleed
Pyelonephritis
Pancreatitis
Uremia
Subdural hematoma
Peripheral vascular occlusion
Any stressor
Common comorbid conditions with HHS
Renal insufficiency, vascular disease, poor access to water
Common associated medications with HHS
Diuretics, B-Blockers, Corticosteroids, Ca++ channel blockers
Phenytoin, Cimetidine
Physical findings for HHS
- Dehydration, Altered, coma rare
Focal neurologic findings
Treatment of HHS
Similar balancing act to DKA
Normal saline(average fluid deficit 8-12 liters)
½ deficit over first 12 hours, the rest over next 24 hours
1-2 liter bolus clinically indicated
Insulin infusion (lower doses than DKA)
Hyperthyroidism causes
-Graves’ disease (most common)-an autoimmune disorder
thyroid-stimulating immunoglobulins mimic TSH action
-Toxic thyroid adenoma, toxic multi-nodular goiter
-Thyroiditis
-Pituitary adenoma
-Drug Induced
-Excess iodine in diet
Hyperthyroidism S/S
Nervousness, tremor, insomnia
Heat intolerance, sweating
Weakness, weight loss, hair loss
Tachycardia, palpitations
Diarrhea
Irregular menses
Goiter / thyroid bruit
Exophthalmos (Graves’ only)
Lid lag (lids move slower than eyes)
Pretibial Myxedema
Thyroid Storm
A life-threatening complication of hyperthyroidism
Essentially a severe form of Thyrotoxicosis
- Most common cause is Graves Disease
Precipitating events for Thyroid storm
Withdrawal of antithyroid meds
Administration of IV contrast
Thyroid hormone overdose
Pneumonia
CVA
Pulmonary embolism
Toxemia of pregnancy
Diabetes
clinical diagnosis of thyroid storm
Hallmark is CNS dysfunction
- Temperature > 38 C
- Tachycardia out of proportion to fever
- Exaggerated peripheral manifestations of thyrotoxicosis
- Including tremor and weakness
- GI-Hepatic Dysfunction
- Atrial Fibrillation
- Congestive Heart Failure
T/F No lab tests distinguish thyroid storm from simple hyperthyroidism
T
5 step treatment approach to Thyroid storm
1)General supportive care-
IV fluids
Correct electrolyte imbalance
No ASA(displaces thyroid hormone from thyroglobulin)
2) Blockade of thyroid hormone synthesis-
- PTU 1000 mg PO (also inhibits peripheral conversion of T4 to T3
3) Blockade of thyroid hormone release
Iodine given 1 hour after PTU
4) 𝛃- adrenergic receptor blockade of peripheral thyroid hormone effects-
- Propranolol
5) Prevent peripheral conversion of thyroxine to triiodothyronine
- Corticosteroids(decrease peripheral conversion T4 to T3)
Hypothyroidism causes
- Treatment of Graves’ disease
- After ablation
- Iodine deficiency in diet
- Autoimmune destruction of thyroid gland
(e.g. Hashimoto’s) - Lithium therapy for bipolar disorder
- Amiodarone
- Pituitary and hypothalamic disorders (rare)
- External Radiation
Hypothyroidism S/S
● Weakness, lethargy
● Cold intolerance
● Hypothermia
● Weight gain
● Constipation
● Dry, thick skin
● Prolonged, heavy periods
● Generalized nonpitting edema
● (myxedema)
Myxedema Crisis (severe hypothyroidism) signs
Dermatologic: Coarse, waxy skin, scant pubic hair,
Loss of lateral third of eyebrows, puffy face and extremities
CNS: Slowed mentation, altered mental status, coma,
psychosis(myxedema madness)
Cardiac: CHF, bradycardia, hypotension, cardiomegaly,
Pericardial effusion, low voltage(ECG)
Hypothyroidism - myxedema coma signs
Non-pitting generalized and periorbital edema
Altered mental status
Hypoxemia
Hypothermia
Bradycardia
Hypotension
Myxedema Coma precipitating factors:
Stressors- MI, infections, trauma, cold exposure
Drugs metabolized slower, increased effects
Non-compliance with thyroid replacement
Myxedema Coma treatment
Supportive care: rewarming, fluid support, underlying cause
Specific treatment
IV thyroxine(T4)- may require large doses
IV T3 is not recommended(causes V- tach)
Corticosteroids- possible unrecognized adrenal/pituitary
Insufficiency
Search for underlying cause
Adrenal Crisis clinical findings
- Acute stressors with underlying insufficiency
- Destruction of hypothalamic-pituitary or adrenal gland
- Hypotension refractory to vasopressors
- Abdominal pain, nausea, vomiting
- Confusion, lethargy
- Look for sepsis
Adrenal Insufficiency treatment
- D5NS IV
- Hydrocortisone
- Pressors
- Future maintenance for anticipated stressors
- Surgery, etc
Adrenal insufficiency labs
Chest X-ray
Abdominal CT to look at Adrenal glands
Brain CT or MRI
HIV Screen
Acute presentation of adrenal insufficiency
Fever and refractory hypotension
Clinical manifestations of adrenal insufficiency
- Cortisol- metabolism of most tissues, glucose regulation
- Aldosterone(renal Na+ reabsorption, K+ excretion)
