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Diabetic and Endocrine
Emergencies
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Diabetes Type I
Usually presents in young patients
Genetic, autoimmune, and/or viral factorscause pancreatic beta islet cell destructionleading to insulin deficiency
Hyperglycemia occurs and can progress to
ketoacidosis if insulin isnt given Symptoms are polyuria, weight loss,
fatigue
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Diabetes Type II
Occurs in older adults
Insulin production may be OK, but the cells areinsulin resistant
Has genetic ties, but diet and obesity determinethe age of onset
Treated with diet, oral hypoglycemics, and insulin Other causes of diabetes: malnutrition,
pancreatitis, endocrine dx, steroid use
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Diabetes Stress-induced hyperglycemia
Can occur in any critically ill patient
Tight control of blood sugar with insulin improves survival
Hypoglycemia Occurs when BS is
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Diabetes Hypoglycemia
Clinical features: Tremor/sweating Progressive confusion
Seizures
Coma/irreversible neurologic damage
Treatment Glucose drink or carb snack if conscious
IV glucose if unconscious
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Diabetes Diabetic ketoacidosis
Occurs with type I diabetes usually from infection,
MI, or pancreatitis Insulin deficiency prevents the cells from taking
glucose upthe kidneys excrete glucose as itbuilds up in the blood which takes water with
itin the meantime, the cells begin to metabolizefat for energy, which produces ketoacids
Clinical presentation: hyperventilation andhypotension/hypoperfusion
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Diabetes Ketoacidosis
Diagnosis Blood sugar Urine dipstick Electrolytes ABG
Management Fluid resuscitation with NS to correct hypovolemia Insulin infusion to reduce blood sugar Electrolyte replacement: especially potassium Acidosis should resolve with fluid and insulin therapy General: O2, ATB, NG tube
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Diabetes Hyperosmolar non-ketotic coma (HONK)
Less common than DKA but has much
higher mortality (~50%) Occurs in elderly patients with Type II who
have sufficienct insulin production toprevent fat metabolism but not
hyperglycemia Osmotic diuresis leads to dehydration and
hyperosmolality, but not ketoacidosis
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Diabetes HONK
Clinical features: anorexia, malaise, polyuria,weakness, confusion, seizures, coma
Diagnosis is based on blood sugar andhyperosmolality
Management Rehydration with NS but more gradually than with DKA Anticoagulants to prevent dehydration-induced emboli
Lactic acidosis Occurs in Type II diabetics treated with
Glucophage
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Endocrine Emergencies Thyroid emergencies
Thyrotoxic crisis is a life-threateninghypermetabolic emergency
Precipitated by infection, surgery, diabetes, labor,radioiodine therapy, and iodinated contrast media
Mortality is ~25%
General management ID and tx the cause
Correct dehydration/electrolyte abnormalities
Avoid aspirin
Cool the patient down/sedate to reduce agitation
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Endocrine Emergencies Clinical features of severe hyperthyroid
CNS: poor concentration, irritability,
confusion, seizures, coma Eyes: lid lag, bulging eyes
Peripheral: tremors, goiter, tachycardia,
jaundice, N&V, heart failure, atrial fib,diarrhea, muscle rigidity/spasm
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Endocrine Thyrotoxic emergency
Specific therapy
Beta blockers: blocks effect of thyroid toreduce HR, HTN, fever, and tremor
Thiourea derivatives: block T4 synthesis
Prevention of T4 release: iodine solutions,
lithium, dexamethasone
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Endocrine Severe hypothyroidism
Occurs with complications to pre-existing
hypothyroidism Causes hypothermia, coma, and
hypotension
Usually affects elderly females withunrecognized hypothyroidism or patientswho fail to take thyroid replacements
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Endocrine Hypothyroidism: clinical features
CNS: lassitude, apathy, coma, seizures
Facial: thin hair, puffy eyes, coarse dry skin,macroglossia
Peripheral: hoarse voice, goiter, bradycarida,weight gain, constipation, urinary retention,
peripheral edema, bradykinesia,hypoventilation/hypoxia, low voltage EKG, flat Twaves, hypoglycemia, hyponatremia
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Endocrine Hypothyroidism
Management Rewarm patient
Support respiratory system
Correct hypoglycemia
IV thyroxine (T4)
Sick euthyroid syndrome Not due to a thyroid disorder Low T4 binding protein and altered T4 metabolism
cause this
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Endocrine
Adrenal emergencies Adrenocortical insufficiency
Reduced cortisol (aldosterone) production by the
adrenal cortex Causes
Adrenal gland destruction Addisons dx Surgical removal Adrenal infarction Infection Infiltration (eg-tumors) Hemorrhage
Secondary Pituitary damage/infarction/hemorrhage Sudden exogenous steroid removal
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Endocrine
Causes of adrenal insufficiency
Hypothalamus destruction
Drugs
Inhibit steroid production
Increase hepatic metabolism
Critical illness
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Endocrine
Clinical presentation of adrenal Acute (Addisonian) crises
Precipitated by stress in patients with unrecognized
adrenal insufficiency, following sepsis, or followingadrenal hemorrhage Pituitary infarction also presents the same way Apathy, hypoglycemia, hypotension, coma Suspect on all patients in shock if the cause is not
apparent
Chronic deficiency Fatigue, weakness, weight loss, fever, and nausea Hyperpigmentation from excessive melanocyte
stimulating hormone production Body hair loss in females from reduced androgen
production
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Endocrine
Adrenal insufficiency Investigation
Low baseline cortisol confirms the diagnosis Hyponatremia, hypoglycemia, hypercalcemia,
eosinophilia are common but not diagnostic ACTH is high in primary adrenal insufficiency and low in
secondary adrenal insufficiency
Treatment If in shock, tx the shock condition (fluids/inotropes) High dose corticosteroids b/c baseline cortisol levels are
low Tx any infection Tx hypoglycemia with glucose
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Endocrine
Adrenocortical excess Cushings syndrome (steroid use) and
Cushings dx (pituitary tumor) increasecortisol levels
Moon face, easily bruised skin, HTN,diabetes, osteoporosis, central obesity, and
hypokalemia Can also have excess aldosterone secretion
with adrenal adenoma
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Endocrine
Other endocrine emergencies Hypopituitary crisis
Follows pituitary trauma/tumor/hemorrhage/ infarction
Reduced anterior pituitary hormone secretion causes adrenaland thyroid insufficiency and hypogonadism
Decreased ADH release from posterior pituitary causes diabetesinsipidus with thirst, dehydration, and severe polyuria
Pheochromocytomas Rare, benign adrenal tumors that release catecholamines
Often familial and there are usually other endocrine tumors
Drugs, surgery, and certain foods can bring on a crisis
HA, sweating, flushing, arrhythmias, HTN, increased plasmacatecholamines
Treat with alpha blockers, beta blockers, and surgery