Clinical Knowledge / Endocrine

Endocrine Emergencies

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Clinical Reference Only. This resource is intended as a study and revision aid. Always verify with current clinical practice guidelines before clinical decision-making.

Endocrine System Overview

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

Key Endocrine Glands — Select to Explore

Click a gland to view its hormones and clinical relevance

Pancreas
Endocrine & Exocrine
Thyroid
Located in neck
Adrenal Glands
Superior to kidneys
Pancreas
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
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Clinical Pearl
Pancreatic juice is inactive inside the pancreas to prevent self-digestion — it only activates upon entry into the duodenum.
Thyroid Gland
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
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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.
Adrenal Glands
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
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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 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.

Interactive BGL Spectrum

Click a segment to view clinical information for that BGL range

HYPO
LOW
NORMAL
HIGH
DKA
HHS
<4 mmol 4–6 4–8 mmol 8–20 mmol 11–33 mmol >33 mmol
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
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Supportive care — position, airway, oxygen as indicated
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IV fluid therapy — support hypovolaemia and dehydration. Caution: rapid bolus can contribute to cerebral oedema in DKA
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Urgent transport — DKA and HHS require definitive hospital management (insulin infusion, electrolyte replacement, monitoring)
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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.

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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 — Stage Stepper

Click each stage to view management steps

1. Assess
2. Conscious
3. IV Access
4. No IV Access
5. Post-Tx
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
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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.

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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
First-line T2DM. Safe in renal impairment down to eGFR ~40.
Prehospital Risk
LOW hypoglycaemia risk — 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 hypoglycaemia risk — 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 hypoglycaemia risk — 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 near-normal BGL). Consider in unwell diabetics on SGLT2 inhibitors.
Note
Avoid in advanced renal impairment. 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 in Australia)
  • More common in older females
  • Post-thyroidectomy or radioiodine therapy
Thyroid Storm — Critical Emergency
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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
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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)
Adrenal Crisis — Critical Emergency
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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 — definitive treatment (100mg IV/IM). Many patients carry an emergency kit
  • 5
    Urgent transport — pre-notify hospital
Cushing Syndrome
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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

Code One Recall — Paramedic Study & Clinical Reference. Always verify with current clinical practice guidelines.