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Endocrine Emergencies

Endocrine assessment and management for paramedicine: how glucose is regulated and what happens at both ends of that scale, the medications that push it there, and the thyroid and adrenal crises that arrive looking like something else.

Endocrine System Overview

Key glands, hormones and their clinical relevance to prehospital practice.

Key Endocrine Glands

Select a gland to see its hormones and why they matter on scene.

Structure

  • Has head, body and tail
  • Ducts lead into the duodenum
  • Acini cells produce pancreatic juices (exocrine)
  • Islets of Langerhans = endocrine portion

Endocrine Hormones

  • Insulin — produced by beta cells; lowers blood glucose
  • Glucagon — produced by alpha cells; raises blood glucose
  • Plays major role in fat digestion and glucose homeostasis

Clinical Pearl

Pancreatic juice is inactive inside the pancreas to prevent self-digestion — it only activates upon entry into the duodenum.

Location & Structure

  • Located in the anterior neck, inferior to the larynx
  • Butterfly-shaped, two lobes connected by isthmus

Hormones Produced

  • Thyroxine (T4) — primary hormone, regulates metabolism
  • Triiodothyronine (T3) — more potent active form
  • TSH (from pituitary) stimulates thyroid hormone release

Physiological Role

T3/T4 regulate basal metabolic rate, heart rate, body temperature, protein synthesis and sensitivity to catecholamines. Dysfunction at either end causes major systemic effects.

Structure

  • Paired glands sitting superior to each kidney
  • Cortex (outer) — steroid hormones
  • Medulla (inner) — catecholamines

Key Hormones

  • Cortisol — stress response, glucose regulation
  • Aldosterone — sodium/potassium balance
  • Adrenaline & Noradrenaline — fight or flight response
  • Androgens — sex hormone precursors

Prehospital Relevance

Adrenal insufficiency impairs the stress response — these patients cannot mount a normal physiological response to illness or trauma, leading to profound shock despite relatively modest illness.

Diabetes Mellitus

Abnormally elevated blood glucose due to absolute or relative insulin deficiency. The most common endocrine emergency encountered in prehospital practice.

Type 1 vs Type 2 — Comparison

Feature Type 1 DM Type 2 DM
Pathophysiology Complete insulin deficiency. 80–90% beta-cell destruction (insulinitis). Immune (genetic) or environmental aetiology. Beta-cell fibrosis. Decreased/defective insulin production + insulin resistance. Strong genetic and lifestyle link. Gradual beta-cell failure.
Age of Onset More common in children and young adults More common in adults; increasing in younger populations with obesity
Insulin Absolute deficiency — lifelong insulin required Relative deficiency — insulin resistance; oral agents often first-line
Acute Emergency Diabetic Ketoacidosis (DKA) Hyperosmolar Hyperglycaemic Syndrome (HHS) — does not typically cause DKA
Symptoms Polyuria, polydipsia, weight loss, Kussmaul breathing, acetone breath, ketonuria, nausea/vomiting Often insidious — polyuria, polydipsia, fatigue, recurrent infections, blurred vision
Diagnosis Fasting BGL >6.9 mmol/L; HbA1c; clinical DKA presentation Fasting BGL >6.9 mmol/L; HbA1c; clinical HHS presentation
Treatment Insulin therapy (lifelong). Prehospital: manage DKA or hypoglycaemia as presenting emergency. Lifestyle modification, oral antihyperglycaemics (Metformin often first-line), insulin if required
Shared Complications Advanced glycosylated end products (AGE) — vascular damage. Neuropathy, nephropathy, retinopathy, CVD, stroke, decreased immunity.

Long-Term Complications

Vascular

  • Cardiovascular disease
  • Stroke
  • Peripheral arterial disease

Microvascular

  • Nephropathy (renal damage)
  • Retinopathy (vision loss)
  • Neuropathy (nerve damage)

Immune

  • Decreased immunity
  • Poor wound healing
  • Increased infection risk

Hyperglycaemia

Elevated blood glucose with differing underlying mechanisms, complications and management approaches.

BGL Spectrum

Select a range to see what it means and what it changes. All values in mmol/L.

Hypoglycaemia — BGL ≤ 4 mmol/L

Inadequate glucose for cellular function. Most common in T1DM. Presents with tachycardia, diaphoresis, ALOC, behaviour mimicking intoxication. Can progress to seizures and coma.
Emergency Treat immediately

Low-Normal — BGL 4–6 mmol/L

Lower boundary of normal range. Monitor closely in patients on insulin or sulphonylureas. May represent resolving hypoglycaemia or a patient trending down.
Monitor

Normal Range — BGL 4–8 mmol/L

Target range for most diabetic patients. Body maintains glucose homeostasis through insulin and glucagon balance. Post-meal levels may reach 10 mmol/L in non-diabetics.
Normal

Hyperglycaemia — BGL 8–20+ mmol/L

Elevated glucose causing osmotic symptoms (polyuria, polydipsia, polyphagia). May indicate poor diabetic control, illness, or medication non-compliance. Monitor for progression to DKA/HHS.
Elevated Supportive care

Diabetic Ketoacidosis (DKA) — Typically 11–33 mmol/L

Insufficient insulin → fat breakdown → ketone production → metabolic acidosis. Typically T1DM. Presents with Kussmaul breathing, acetone breath, ALOC, vomiting. Life-threatening.
Critical T1DM typical Acidosis

Hyperosmolar Hyperglycaemic Syndrome (HHS) — BGL >33 mmol/L

Severe hyperglycaemia without significant ketoacidosis. Insulin still present but insufficient. Profound dehydration and hyperosmolarity. Life-threatening emergency. Typically T2DM. Gradual onset.
Life-threatening T2DM typical Dehydration

DKA vs HHS — Comparison

Diabetic Ketoacidosis (DKA)

Key Features

  • Usually Type 1 DM
  • Insufficient insulin → excess ketone production
  • Blood becomes acidic (metabolic acidosis)
  • BGL typically 11–33 mmol/L

Symptoms

  • ALOC, confusion, coma
  • Kussmaul respirations (deep, rapid breathing)
  • Acetone/fruity breath
  • Nausea, vomiting, abdominal pain
  • Dehydration
Hyperosmolar Hyperglycaemic Syndrome (HHS)

Key Features

  • Usually Type 2 DM
  • Insulin still present — no significant ketosis
  • Severe dehydration and hyperosmolarity
  • BGL > 33 mmol/L

Symptoms

  • ALOC, confusion, coma
  • Gradual onset over days
  • Profound dehydration
  • No Kussmaul breathing
  • No ketones/acetone smell

Hyperglycaemia Management

Confirm hyperglycaemia via BGL measurement
↓
Supportive care — position, airway, oxygen as indicated
↓
IV fluid therapy — support hypovolaemia and dehydration. Caution: rapid bolus can contribute to cerebral oedema in DKA
↓
Urgent transport — DKA and HHS require definitive hospital management (insulin infusion, electrolyte replacement, monitoring)

Alcoholic Ketoacidosis

Occurs in chronic alcoholics following binge drinking and reduced oral intake. Presents with tachypnoea, BGL <11 mmol/L, dehydration, and ketonuria. Often overlooked — consider in patients who appear intoxicated.

Hypoglycaemia

BGL ≤ 4 mmol/L. One of the most common endocrine emergencies in prehospital practice — easily treatable but rapidly life-threatening if missed.

Critical Reminder

Hypoglycaemia can mimic intoxication, CVA, and psychiatric presentations. Always check BGL in any patient with altered LOC, unusual behaviour, or suspected stroke.

Causes

  • Typically affects T1DM patients
  • Insulin overdose
  • Insulin administered without subsequent meal
  • Excessive physical exertion
  • Sulphonylurea medications (T2DM)
  • Alcohol intake (inhibits gluconeogenesis)

Clinical Presentation

  • Tachycardia with bounding pulse
  • Pale, cold, clammy skin
  • ALOC — ranging from confusion to coma
  • Irritability, aggression, personality change
  • Behaviour mimicking intoxication or CVA
  • Seizure activity
  • Diaphoresis, tremor, hunger

Management

Five stages, in the order you work through them.

Assessment

  • Confirm BGL ≤ 4 mmol/L via glucometer
  • Assess level of consciousness (GCS/AVPU)
  • Check for medical alert bracelet
  • Obtain medication history — insulin, sulphonylureas
  • Consider mimics: CVA, overdose, sepsis

Conscious Patient — Can Swallow

  • Oral glucose — glucose gel, sugary drink, jelly beans
  • Oral carbohydrates — follow with a complex carbohydrate snack (e.g. toast)
  • Recheck BGL after 10–15 minutes
  • Continue monitoring until BGL stabilises >4 mmol/L

IV Access Established

  • IV Glucose 10% — preferred in unconscious or unable to swallow
  • Titrate to BGL response — recheck every 5–10 mins
  • Ensure IV access is patent before administration
  • Once responsive — follow up with oral carbohydrates

No IV Access — Unconscious

  • Glucagon IM/SC — stimulates hepatic glucose release
  • Not very effective for paediatric patients
  • Requires adequate glycogen stores — may be ineffective in malnourished, chronic alcohol users
  • Continue attempts to establish IV access while awaiting response

Post-Treatment

  • Recheck BGL to confirm response — target >6 mmol/L
  • Provide complex carbohydrate meal to prevent rebound
  • Advise patient to review insulin dosing with GP
  • Sulphonylurea-induced hypoglycaemia may rebound — consider transport for observation
  • Document BGL before and after treatment

Paediatric Considerations

Paediatric Hypoglycaemia

In paediatric patients with hypoglycaemia, always consider other causes: concurrent illness, sepsis, poisoning, or metabolic disorders. Glucagon is less effective in children. IV glucose is preferred definitive treatment.

Gestational Diabetes

Pathophysiology

  • Increased insulin resistance during pregnancy
  • Beta cell dysfunction
  • Affects approximately 6% of pregnancies

Clinical Relevance

  • Risk of hypoglycaemia if managing insulin in pregnancy
  • Large-for-gestational-age fetus
  • Usually resolves after delivery but increases T2DM risk

Glucose-Lowering Medications

Understanding common diabetic medications is essential for predicting adverse effects — particularly hypoglycaemia risk — in prehospital encounters.

Prehospital Relevance

Insulin and sulphonylureas carry the highest risk of hypoglycaemia. Always obtain a medication history in any patient with ALOC or unusual behaviour. Document which medications the patient is on.

Mechanism
Improves insulin sensitivity in muscle and reduces hepatic glucose output.
Indication
Often first-line in T2DM. Safe in renal impairment down to eGFR ~40.
Prehospital risk
Low
Does not stimulate insulin secretion.
Note
Hold around contrast media. Avoid in severe renal failure.

Mechanism
Stimulate insulin secretion from beta cells regardless of blood glucose level.
Examples
Glibenclamide, glipizide, gliclazide, glimepiride.
Prehospital risk
High
Can cause prolonged, rebound hypoglycaemia. Consider hospital transport for observation.
Note
Weight gain. Short-acting agents preferred in renal impairment.

Mechanism
Replaces declining endogenous insulin. Controls glucose when oral agents fail.
Types
Rapid-acting (aspart, lispro), short-acting (regular), intermediate (NPH), long-acting (glargine, detemir).
Prehospital risk
High
Especially rapid-acting insulin. Insulin errors are a leading cause of prehospital hypoglycaemia.
T1DM use
Lifelong — cannot be omitted. Omission leads to DKA.

Mechanism
Block renal glucose reabsorption, causing glycosuria, weight loss and mild diuresis.
Examples
Empagliflozin, dapagliflozin, canagliflozin.
Prehospital risk
Moderate
Can cause euglycaemic DKA — DKA with a near-normal BGL. Consider it in any unwell diabetic taking one.
Note
Avoid in advanced renal impairment. Often second-line after metformin.

Drug ClassExamplesMechanismHypo Risk
GLP-1 AgonistsExenatide, liraglutide, semaglutideEnhance glucose-dependent insulin, slow gastric emptying, aid weight lossLow
DPP-4 InhibitorsSitagliptin, saxagliptinIncrease incretin hormones (GLP-1, GIP)Low
TZDsPioglitazone, rosiglitazoneImprove insulin sensitivity in muscle and liverLow
AcarboseAcarboseInhibits intestinal carbohydrate absorptionLow

Thyroid Emergencies

Thyroid dysfunction affects multiple organ systems. Extreme presentations — thyroid storm and myxoedema coma — are life-threatening emergencies.

Hyperthyroidism vs Hypothyroidism

Hyperthyroidism — Excess T3/T4

Signs & Symptoms

  • Tachycardia, palpitations, AF
  • Exophthalmos (abnormal eye protrusion)
  • Agitation, anxiety, delirium
  • Fatigue, heat intolerance, diaphoresis
  • Weight loss despite increased appetite
  • Abdominal pain, diarrhoea
  • Fine tremor

Common Causes

  • Graves' disease (most common)
  • Toxic multinodular goitre
  • Excess thyroid hormone intake
Hypothyroidism — Deficient T3/T4

Signs & Symptoms

  • Bradycardia, hypotension
  • Fatigue, lethargy, cold intolerance
  • Weight gain, constipation
  • Dry skin, hair loss, hoarseness
  • Depression, cognitive slowing
  • Periorbital and peripheral oedema
  • Myxoedema (non-pitting oedema)

Common Causes

  • Autoimmune thyroiditis (most common cause in iodine-replete regions)
  • More common in older females
  • Post-thyroidectomy or radioiodine therapy

Thyroid Storm — Critical Emergency

Life-Threatening Emergency

Thyroid storm is a rare but life-threatening exacerbation of hyperthyroidism. Mortality is high without rapid identification and treatment. Most commonly triggered by illness, surgery, or medication non-compliance.

Signs & Symptoms

  • High fever — temperature >38.5°C
  • Severe tachycardia — may develop AF
  • Heart failure, haemodynamic instability
  • Confusion, disorientation, agitation
  • Nausea, vomiting, diarrhoea
  • Weakness, tremor
  • Diaphoresis, warm skin

Prehospital Management

  • 1
    Recognise — fever + severe tachycardia + delirium in known or suspected thyroid disease
  • 2
    Airway, O2 & IV access — supportive care, monitor SpO2
  • 3
    Cooling measures — tepid sponging, remove excess clothing, cool environment
  • 4
    IV fluids — dehydration support; monitor for cardiac compromise
  • 5
    Cardiac monitoring — high risk of AF and arrhythmia
  • 6
    Urgent transport — pre-notify hospital; in-hospital Rx includes beta-blockers, antithyroid drugs, iodine, corticosteroids

Myxoedema Coma

Severe Hypothyroidism Emergency

Myxoedema coma is the extreme, life-threatening end of hypothyroidism. High mortality. Often triggered by cold, infection, or medication non-compliance.

Presentation

  • Decreased or absent consciousness
  • Hypothermia — core temperature may be very low
  • Bradycardia, hypotension
  • Respiratory depression / hypoventilation
  • Periorbital and facial oedema

Prehospital Management

  • 1
    Recognise — hypothermia + ALOC + bradycardia in known or suspected hypothyroid patient
  • 2
    Airway management — support ventilation as required; high aspiration risk
  • 3
    Passive rewarming — warm blankets; avoid aggressive active rewarming
  • 4
    IV access & fluids — cautious fluid support for hypotension
  • 5
    Cardiac monitoring — bradyarrhythmia risk
  • 6
    Urgent transport — pre-notify hospital

Adrenal Emergencies

Adrenal gland dysfunction can result in life-threatening hormonal crises — adrenal insufficiency impairs the stress response, while Cushing syndrome reflects prolonged cortisol excess.

Adrenal Insufficiency

Addison's Disease (Primary)

  • Autoimmune destruction of adrenal cortex
  • Insufficient cortisol and aldosterone
  • Chronic presentation: fatigue, weight loss, hyperpigmentation
  • Postural hypotension, salt craving
  • Hyperkalaemia, hyponatraemia

Secondary Adrenal Insufficiency

  • Pituitary dysfunction — insufficient ACTH
  • Long-term corticosteroid use (suppresses HPA axis)
  • Abrupt steroid withdrawal — can precipitate crisis
  • No hyperpigmentation (unlike Addison's)

Hyperkalaemia — ECG Progression

Why this matters here

Addison's disease and adrenal crisis cause hyperkalaemia (loss of aldosterone). A rising potassium changes the ECG in a recognisable sequence — peaked T waves are the earliest sign, and untreated hyperkalaemia can progress through a broad, bizarre QRS to a pre-terminal sine wave and cardiac arrest.
1Peaked T wavesK⁺ ~5.5–6.5
Earliest change: tall, narrow-based, symmetric "tented" T waves. It is the narrow, pinched base — not just the height — that distinguishes them from a benign tall T. P wave, PR and QRS still normal.
2ModerateK⁺ ~6.5–7.5
Peaked T persists, and now the P wave flattens, the PR interval lengthens, and the QRS begins to widen.
3SevereK⁺ ≥7.5
The P wave disappears and the QRS becomes broad, bizarre and slurred, starting to merge with the T wave.
4Sine wave — pre-terminalK⁺ >9
The widened QRS and T fuse into a continuous sine wave. This is a peri-arrest rhythm — it precedes ventricular fibrillation, PEA and asystole. Treat immediately.

How to read these

Idealised teaching diagrams in lead II, generated from a waveform model — not real patient recordings, and not a substitute for a 12-lead ECG. Peaked T waves are most dramatic in the chest leads (V2–V4).

Adrenal Crisis — Critical Emergency

Life-Threatening Emergency

Adrenal crisis is characterised by severe cortisol deficiency. Patients cannot mount a normal stress response. Can be rapidly fatal. Often triggered by infection, trauma, surgery, or steroid withdrawal.

Presentation

  • Profound hypotension / shock — refractory to fluids
  • ALOC, confusion, coma
  • Severe nausea, vomiting, abdominal pain
  • High fever or hypothermia
  • Hypoglycaemia
  • Weakness, fatigue

Prehospital Management

  • 1
    Recognise — known Addison's/steroid user + haemodynamic instability
  • 2
    IV access & fluids — aggressive normal saline for hypotension
  • 3
    Dextrose — if hypoglycaemia present
  • 4
    Hydrocortisone (IV/IM) — definitive treatment. Many patients carry an emergency kit
  • 5
    Urgent transport — pre-notify hospital

Cushing Syndrome

Cortisol Excess

Cushing syndrome results from prolonged excess cortisol — most commonly from long-term corticosteroid use (iatrogenic), or from a cortisol-secreting tumour (adrenal or pituitary).

Classic Features

  • Central obesity with thin limbs
  • Buffalo hump (fatty hump on upper back)
  • Moon face (rounded, plethoric)
  • Purple striae (stretch marks) on abdomen
  • Hypertension, hyperglycaemia
  • Osteoporosis, proximal muscle weakness

Prehospital Considerations

  • May present with uncontrolled hypertension or hyperglycaemia
  • Fragile skin — careful with IV access and packaging
  • Immunosuppressed — high infection risk
  • Often on corticosteroids — adrenal crisis risk if steroids missed

Keep going

Reading it through once is the easy part. These are the ways to make it stick.

Test yourself Daily question One clinical question a day, with a streak to keep. Drill it Flashcards Spaced repetition that brings a card back before you forget it. Go deeper Neurological Altered consciousness and the stroke mimics — where an untested BGL does the most damage.