Emergency Medicine Lecture 2

What is the etiology of hypoglycemia?

Insulin/sulfonylureas, missed meals, alcohol, sepsis, renal failure, and adrenal insufficiency.

What are the clinical symptoms of hypoglycemia?

Diaphoresis, tremor, tachycardia, hunger, anxiety, confusion, seizure, and coma.

How is hypoglycemia diagnosed in the emergency department?

Bedside glucose test showing levels usually <70 mg/dL; classified as severe if altered mental status or seizures occur.

What is the ED management protocol for hypoglycemia?

Oral glucose if awake; IV dextrose if altered; IM/IN glucagon if no IV. Observe longer for sulfonylureas and consider octreotide.

What are the potential complications of hypoglycemia?

Seizures, coma, aspiration, cardiac arrhythmia, and death.

What is the etiology of hyperglycemia in the ED?

Diabetes, infection, myocardial infarction, stroke, steroids, and medication nonadherence.

What are the classic symptoms of hyperglycemia?

Polyuria, polydipsia, dehydration, blurred vision, and weakness.

What laboratory tests must be ordered to evaluate a hyperglycemic patient for DKA or HHS?

BMP, anion gap, serum/urine ketones or beta-hydroxybutyrate, venous pH, and osmolality.

What is the initial ED management for general hyperglycemia?

IV fluids first, electrolyte correction, insulin when appropriate, and treating the underlying trigger.

What is the etiology of Diabetic Ketoacidosis (DKA)?

Absolute insulin deficiency, infection, MI, missed insulin, new-onset type 1 DM, or SGLT2 inhibitors.

What are the symptoms of Diabetic Ketoacidosis (DKA)?

Polyuria, dehydration, nausea/vomiting, abdominal pain, Kussmaul respirations, fruity breath, and altered mental status.

How is Diabetic Ketoacidosis (DKA) diagnosed?

Hyperglycemia (usually >250 mg/dL), anion gap metabolic acidosis, and positive ketones/beta-hydroxybutyrate.

What is the ED management sequence for Diabetic Ketoacidosis (DKA)?

IV isotonic fluids, potassium assessment/repletion, IV insulin (after potassium is safe), dextrose when glucose falls, and treating triggers.

What are the complications of Diabetic Ketoacidosis (DKA)?

Cerebral edema, hypokalemia, cardiac arrhythmia, and shock.

What is the etiology of Hyperosmolar Hyperglycemic State (HHS)?

Type 2 DM, elderly age, infection, severe dehydration, stroke/MI, and steroids.

What are the typical symptoms of Hyperosmolar Hyperglycemic State (HHS)?

Severe dehydration, weakness, confusion, seizures, and coma.

How is Hyperosmolar Hyperglycemic State (HHS) diagnosed?

Very high glucose (often >600 mg/dL), high serum osmolality, and little or no ketoacidosis.

What is the ED management for Hyperosmolar Hyperglycemic State (HHS)?

Aggressive IV fluids, potassium correction, insulin after initial fluid resuscitation, and treating the precipitant.

What are the main complications of Hyperosmolar Hyperglycemic State (HHS)?

Thrombosis, seizures, coma, shock, and death.

How do DKA and HHS compare regarding typical patient profile and onset?

DKA: younger type 1 DM patients, rapid onset (hours-1 day). HHS: older type 2 DM patients, slower onset (days-weeks).

How do DKA and HHS compare regarding blood glucose and ketone levels?

DKA: glucose >250 mg/dL, moderate-large ketones. HHS: glucose >600 mg/dL, minimal/absent ketones.

How do DKA and HHS compare regarding pH, bicarbonate, and anion gap?

DKA: low pH, low HCO3, elevated anion gap. HHS: pH >7.30, HCO3 >18, normal/mildly elevated anion gap.

How do DKA and HHS compare regarding serum osmolality and dehydration severity?

DKA: elevated osmolality, moderate-severe dehydration. HHS: markedly elevated osmolality, profound dehydration.

How do DKA and HHS compare regarding mental status changes?

DKA: variable mental status. HHS: common and severe altered mental status.

How do DKA and HHS fluid and insulin therapy timing differ?

DKA: IV insulin after potassium check. HHS: fluids first, then insulin.

What is the typical disposition for DKA vs HHS?

DKA: ICU or stepdown depending on severity. HHS: usually ICU or stepdown.

What labs should be ordered for suspected Alcoholic Ketoacidosis (AKA)?

CBC, chemistry panel, ABG, and serum beta-hydroxybutyrate or urine ketones.

What laboratory findings are classic for Alcoholic Ketoacidosis (AKA)?

Elevated anion gap metabolic acidosis, presence of ketone bodies, hypokalemia, hypophosphatemia, hypomagnesemia, and an elevated serum osmolal gap.

How do the typical patient and trigger compare between AKA and DKA?

AKA: chronic alcohol user after a binge followed by poor oral intake/vomiting. DKA: type 1 diabetic triggered by infection, missed insulin, or MI.

How do blood glucose levels compare between AKA and DKA?

AKA: normal or mildly elevated (<250 mg/dL). DKA: usually >250 mg/dL (often >350-600 mg/dL).

How do insulin levels compare between AKA and DKA?

AKA: low-normal insulin levels. DKA: markedly deficient insulin levels.

How do ketones and acidosis compare between AKA and DKA?

Both present with elevated ketones (beta-hydroxybutyrate predominates) and a high anion gap metabolic acidosis.

How do mental status and volume status compare between AKA and DKA?

AKA: usually alert despite severe acidosis, dehydrated. DKA: ranges from alert to coma, severely dehydrated.

How do serum ethanol levels compare at presentation in AKA vs DKA?

AKA: may be low or undetectable. DKA: not related.

What is the fluid resuscitation protocol for Alcoholic Ketoacidosis?

Administer D5NS IV until rehydrated, then D5 0.45NS IV for maintenance.

Why must thiamine be given in AKA, and what is the sequence relative to glucose?

Give thiamine 100 mg IV prior to glucose to prevent worsening of Wernicke's encephalopathy.

When should bicarbonate therapy be considered in AKA?

Consider bicarbonate only if the pH remains <7.0 after initial hydration.

What is the correct clinical intervention for a patient with AKA, normal glucose, and elevated beta-hydroxybutyrate?

IV thiamine followed by dextrose-containing IV fluids.

What is the difference between thyrotoxicosis and hyperthyroidism?

Thyrotoxicosis: any condition of excessive thyroid hormone. Hyperthyroidism: hyper-functioning of the thyroid gland itself.

What are the common causes of hyperthyroidism in young vs elderly patients?

Young: Graves disease. Elderly: Toxic nodular goiter.

What is the etiology of thyrotoxicosis and thyroid storm?

Graves disease, toxic multinodular goiter, or thyroiditis; triggered by infection, surgery, trauma, MI, childbirth, or medication nonadherence.

What are the symptoms of thyroid storm?

Fever, agitation/delirium, tachycardia/atrial fibrillation, hypertension progressing to shock, diarrhea/vomiting, and tremor.

How is thyroid storm diagnosed?

Clinical diagnosis; supported by low TSH and elevated free T4/T3. Do not wait for labs if unstable.

What are the potential complications of thyroid storm?

Arrhythmias, heart failure, shock, and death.

What is the sequential drug therapy for managing thyroid storm in the ED?

1. Beta-blocker (propranolol/esmolol), 2. Thionamide (PTU/methimazole), 3. Iodine (at least 1 hour after thionamide), 4. Steroids (hydrocortisone).

What is the etiology of hypothyroidism and myxedema coma?

Severe untreated hypothyroidism; triggered by infection, cold exposure, sedatives/opioids, trauma, or MI.

What are the classic symptoms of myxedema coma?

Altered mental status, hypothermia, bradycardia, hypotension, hypoventilation, hyponatremia, and hypoglycemia.

How is primary myxedema coma diagnosed?

Clinical presentation of hypothermia, bradycardia, and AMS; supported by high TSH and low free T4.

What is the ED management for myxedema coma?

Airway/ventilation, warming, IV levothyroxine, stress-dose steroids before/with thyroid hormone, and correcting sodium/glucose.

What are the potential complications of myxedema coma?

Respiratory failure, shock, coma, and death.

What is the etiology of adrenal crisis (acute adrenal insufficiency)?

Addison's disease, chronic steroid withdrawal, pituitary disease, sepsis, or adrenal hemorrhage.

What are the symptoms of adrenal crisis?

Shock, hypotension refractory to fluids/pressors, vomiting, abdominal pain, weakness, fever, and confusion.

What laboratory findings are characteristic of primary adrenal failure?

Hyponatremia, hyperkalemia, hypoglycemia, and eosinophilia.

What is the ED management for adrenal crisis?

Draw cortisol/ACTH (do not delay care); give hydrocortisone 100 mg IV/IM immediately, IV normal saline, and dextrose if hypoglycemic.

What are the complications of an adrenal crisis?

Refractory shock, cardiac arrhythmias, and death.

What is the etiology of central vs nephrogenic diabetes insipidus?

Central: head trauma, pituitary surgery/tumor. Nephrogenic: lithium use, hypercalcemia, hypokalemia.

What are the symptoms of diabetes insipidus?

Polyuria, polydipsia, dehydration, hypernatremia, and altered mental status.

How is diabetes insipidus diagnosed?

High serum sodium and high serum osmolality with inappropriately dilute urine.

What is the ED management for diabetes insipidus?

Volume resuscitation if unstable, slow free water correction, desmopressin for central DI, and treating the cause.

What are the complications of diabetes insipidus?

Severe hypernatremia, seizures, and coma.

What is the etiology of SIADH?

CNS disease, pulmonary disease, malignancy, SSRIs, carbamazepine, antipsychotics, pain, or nausea.

What are the symptoms of SIADH?

Nausea, headache, confusion, seizures, and coma.

How is SIADH diagnosed?

Hyponatremia, low serum osmolality, inappropriately concentrated urine, elevated urine sodium, and clinical euvolemia.

What is the ED management for SIADH?

Fluid restriction if mild; 3% hypertonic saline for seizures, coma, or severe symptoms. Avoid rapid correction.

What are the complications of SIADH?

Cerebral edema, or osmotic demyelination syndrome (from overcorrection).

What is the etiology of hyperparathyroidism and hypercalcemic crisis?

Primary hyperparathyroidism, malignancy, lithium, and granulomatous disease.

What are the symptoms of hypercalcemic crisis?

"Stones, bones, groans, psychiatric overtones"; dehydration, constipation, abdominal pain, weakness, confusion, shortened QT, and arrhythmias.

How is hypercalcemic crisis diagnosed?

Elevated serum calcium, elevated ionized calcium, PTH levels, renal function tests, and ECG changes.

What is the ED management for hypercalcemic crisis?

Aggressive IV normal saline, calcitonin, bisphosphonates (for malignancy), loop diuretics (only after rehydration), or dialysis.

What are the complications of hyperparathyroidism and hypercalcemic crisis?

Renal failure, cardiac arrhythmias, pancreatitis, and coma.

In severe DKA, why must potassium levels be addressed before starting insulin?

Insulin drives potassium intracellularly; starting insulin when serum potassium is <3.3 mEq/L can precipitate fatal arrhythmias.

What is the correct action if a DKA patient's potassium is 3.1 mEq/L?

Administer IV KCl and hold insulin therapy until serum potassium is >3.3 mEq/L.

What three questions should always be asked and answered before discharging an ED patient?

1. Why did the patient come to the ED? 2. Have all specific concerns/fears been addressed? 3. Have I made the patient feel better?

What is the general approach to acute pain control in the ED?

Assess severity, location, mechanism, allergies, organ function, and use multimodal nonopioid analgesia when possible.

What are the indications and adverse effects of Acetaminophen?

Indications: mild-moderate pain, fever. Adverse effects: hepatotoxicity. Avoid in severe liver disease.

What are the indications and adverse effects of NSAIDs (Ibuprofen/Ketorolac)?

Indications: MSK, renal colic, dental pain. Adverse effects: AKI, GI bleed, platelet dysfunction. Avoid in CKD/pregnancy.

What are the indications and adverse effects of Opioids (Morphine, Fentanyl, Hydromorphone)?

Indications: severe acute pain, fractures, burns, trauma. Adverse effects: respiratory depression, hypotension, sedation, constipation.

What are the indications and adverse effects of low-dose Ketamine?

Indications: severe pain, opioid tolerance, trauma. Adverse effects: dysphoria, nausea, hypertension, emergence reactions.

What is the classic triad of opioid toxicity?

Coma, miosis (pinpoint pupils), and respiratory depression.

What is the primary treatment and goal for opioid overdose?

Ventilation support and Naloxone (Narcan). The goal is return of adequate spontaneous respirations to ventilate safely.

What is the onset and duration of action of Naloxone (Narcan)?

Onset is 2-5 minutes; duration is 30-60 minutes (may require re-dosing).

What are the discharge instructions for a patient taking sedating pain medications?

Avoid making important decisions, operating machinery, climbing heights, swimming alone, or cooking over an open flame.

What are the four levels of sedation defined in procedural sedation?

Minimal (normal response), Moderate (verbal/tactile response), Deep (painful response), and General Anesthesia (unarousable).

What are the clinical indications for procedural sedation in the ED?

Reduction of fractures/dislocations, cardioversion, abscess drainage, complex laceration repair, burn care, and foreign body removal.

What monitoring is required during ED procedural sedation?

Continuous pulse oximetry, cardiac monitor, blood pressure, respiratory assessment (preferably capnography), and IV access.

What are the benefits and concerns of Ketamine as a sedation agent?

Benefits: preserves respiratory drive. Concerns: emergence reaction, vomiting, rare laryngospasm.

What are the benefits and concerns of Propofol as a sedation agent?

Benefits: rapid onset and offset. Concerns: hypotension and respiratory depression.

What are the benefits and concerns of Etomidate as a sedation agent?

Benefits: hemodynamic stability. Concerns: myoclonus and transient adrenal suppression.

What are the benefits and concerns of Midazolam as a sedation agent?

Benefits: anxiolysis and amnesia. Concerns: respiratory depression and prolonged sedation.

What are the properties of Lidocaine vs Lidocaine with epinephrine?

Lidocaine: fast onset, short-moderate duration. With epinephrine: longer duration, less bleeding (avoid in compromised circulation).

What are the clinical signs and treatment of Local Anesthetic Systemic Toxicity (LAST)?

Perioral numbness, tinnitus, metallic taste, seizures, arrhythmias. Treat with airway support, benzodiazepines, and lipid emulsion.

What is the ED treatment plan for chronic pain exacerbations?

Rule out new emergencies, use nonopioid multimodal therapy, avoid routine IV opioids, do not replace lost/stolen prescriptions, check PDMP.

What are the three types of wound closure?

Primary intention (immediate closure), Secondary intention (left open to heal), and Tertiary intention (delayed primary closure).

How does suture sizing work?

Sizes run from 7-0 to 1-0. A smaller number before the dash means a thicker suture (e.g., 3-0 is thicker than 5-0).

What are the standard suture sizes for the face, extremities, and high-tension areas?

Face (cosmetically sensitive areas): 6-0 or 5-0. Extremities/Trunk/Scalp: 4-0. High-tension areas: 3-0.

What are the common nonabsorbable suture types used for skin closure?

Nylon and Prolene (both monofilaments with low tissue reaction).

What are the general steps in laceration management?

Pain control, irrigation, exploration, foreign body removal.

What are the key management pearls for facial lacerations?

Use 5-0 or 6-0 sutures; do not shave eyebrows; align the vermilion border of the lip first; remove sutures early (3-5 days).

What are the advantages and disadvantages of staples?

Advantage: Speed and relative ease of use and cost effective. Disadvantage: Allows least amount of precision. Should only be used in linear wounds!

What are the indications and contraindications for Dermabond (skin adhesive)?

Indications: small, clean, linear, low-tension wounds. Contraindications: jagged/high-tension wounds, bites, punctures, mucosal/wet areas.