ENDOCRINOLOGY

Diabetic ketoacidosis

→ A complex disordered metabolic state characterised by Hyperglycaemia, Ketonaemia and

Acidosis (HAGMA)

⇒ Causes:
● Infection (Meningitis, Pyelonephritis etc)
● Infraction (MI, CVA, Ischemic colitis etc)
● Intercurrent illness (IBS)
● Insufficient insulin (When not taking insulin properly)

⇒ The diagnostic criteria for DKA are:

1. Ketonemia (beta-hydroxybutyrate) (>3 mmol/L) or significant ketonuria (>2+ on urine dipstick)
2. Blood glucose >11 mmol/L or known diabetes mellitus
3. Bicarbonate <15 mmol/L and/or venous pH <7.3

⇒ Clinical features:
● Hyperglycaemia typically results in thirst, polyuria, and polydipsia.
● Cardiovascular—hypotension and tachycardia due to dehydration.
● Gastrointestinal—abdominal pain, nausea, and vomiting.
● Respiratory—Kussmaul’s breathing
● Neurological—altered conscious level, confusion, focal neurology, and coma.

→ Osmotic diuresis → Dehydration → Shock, Tachycardia

→ Inc RR → Inc CO2 washout → Acetone breath, Acidosis + Ketone bodies → Altered GCS

⇒ Investigations: For diagnosis and complications

● Blood ketones
● VBG: Ph
● Blood sugar levels
● Urea and creatinine: Any renal or electrolyte abnormality
● FBC/urine analysis/ cultures/ CXR: To see any infection
● ECG/ Trop-I
● CT brain

⇒ Management:
● A/B: When GCS < 7: Ventilation. Otherwise, Low O2: OPA followed by O2
● C
 ● If the patient usually takes long-acting insulin (e.g. detemir or glargine) this should be
continued at the usual dose and time. Pt using an Insulin pump / SA insulin, it should be
stopped before starting the DKA protocol

● Potassium chloride: Initially, K will be high as there is Metabolic acidosis. So, K comes out
of the cell in exchange for H. However, it will be reduced once Inf Insulin is started. Keep K
level in hand before Insulin infusion.
The followings are the K replacement requirement in the infusion fluid. (from 2nd bag of fluid)

➔ K > 5.5: Nil

➔ K 3.5 - 5.5: 40mmol
➔ K < 3.5: 60-80 mmol/L (HDU support required)

⇒ Complications:
● Hypokalaemia and hyperkalaemia: Close monitoring is required
● Hypoglycaemia
● Cerebral oedema: When IVF is given rapidly (Especially in Children)
● Pulmonary oedema: When more fluid is given in CCF pt
● Aspiration pneumonia: Securing the airway is needed in low GCS pt.

PEDS- Diabetic ketoacidosis (BSPED)

⇒ Investigations: Similar to the adults

● Blood ketones
● VBG: Ph
● Blood sugar levels
● Urea and creatinine: Any renal or electrolyte abnormality
● FBC/urine analysis/ cultures/ CXR: To see any infection
● ECG/ Trop-I
● CT brain
⇒ Treatment: DKA management summary

Adult Paediatric

Fluid Shock 500 - 1000 ml NS over 10-15min 10ml/kg every 15 min

No Shock • 1L NS over 1hr • 10ml/kg over 30 min (slow bolus)

• 1L NS with KCl over 2hr • Requirement= Deficit (over 48 hr) +
• 1L NS with KCl over 2hr Maintenance (over 24hr) – 10ml/kg (slow
bolus given in non-shock patient)

Insulin infusion 0.1 U/kg/hr (70 kg pt will be started on • 0.05 U/kg/hour after 1-2 hours of IVF
7U/hr, MC used insulin Human Actrapid • Severe DKA & adolescent- 0.1 U/kg/hr
and Insulin inf will reduce ketone after 1-2 hours IVF
production)

Increase insulin By 1U/hour if NO ↓ Ketones 0.5 mmol/L/hr

Potassium • >5.5: nil • >5.5: 40 mmol/litre added to fluids after

correction • 3.5-5.5: 40 mmol/L the patient passed urine
• <3.5: 60-80 mmol/L (HDU support) • 3 – 5.5: 40 mmol/litre added to fluids
• <3: 40 mmol/litre to fluids+ insulin
deferred till K+ > 3mmol/L

If BM <14mmol/L Start 10% dextrose @ 125 ml/hr • Change the fluid to 5% glucose.
• ↓ insulin infusion rate to 0.05 U/kg/hr, if
started at 0.1 U/kg/hr

Monitoring • Capillary ketones and Glucose- 1hrly • Blood ketones and capillary glucose- 1hrly
• pH and bicarbonate- 1 hrly for 1st 2hr • Urea and electrolytes, bicarbonate, blood
then 2hrly pH, and laboratory glucose- after 2 hr then
• Electrolytes- 4hrly 4 hrly

Requirement = Deficit + Maintenance

Deficit: The deficit should be replaced over 48 hours
Deficit = Fluid deficit x weight (kg) x 10 / 48 hrs
pH 7.1 to 7.29 = 5 fluid deficit
pH < 7.1 = 10 fluid deficit

Maintenance fluid:
100 ml/kg/day for the 1st 10 kg of BW
50 ml/kg/day for the next 10-20 kg
20 ml/kg/day for each additional kgs above 20 kg

Requirement = Deficit + Maintenance

Deficit:
• Deficit should be replaced over 48 hours
• Resuscitation fluid –
• The volume of any fluid boluses given for resuscitation in children with shock should NOT be
subtracted from the estimated fluid deficit.
• The initial 10ml/kg bolus given to all non-shocked patients requiring IV fluids SHOULD be
subtracted from a total calculated fluid deficit.
→ A 20 kg 6-year-old boy who has a pH of 7.15 (Moderate DKA => 5% Dehydrated) will receive a 10ml/kg
bolus (200mls fluid) over 30 minutes as part of his initial management. His ongoing fluids will comprise:

⇒ POTASSIUM:
• Ensure that every 500 ml fluid bag contains 20 mmol potassium chloride (40 mmol per litre).

⇒ INSULIN:
• Start an intravenous insulin infusion 1-2 hours after beginning intravenous fluid therapy.

• For children and young people on continuous subcutaneous insulin infusion (CSII) pump therapy,
stop the pump when starting intravenous insulin.

• For children who are already on long-acting insulin, you may wish to continue this at the usual
dose and time throughout the DKA treatment, in addition to the IV insulin infusion

• Do not give intravenous sodium bicarbonate to children and young people with DKA
 Complication: Cerebral Oedema

⇒ Clinical features:
● Headache, irritability
● Slowing HR
● Reduced GCS / coma
● Signs of raised ICP
● Others as show on care pathway

⇒ Management:
● Give 5ml/kg 2.7% NaCl Or 20% Manitol 2.5-5 ml/kg
● Call senior staff
● Restrict IVF by 50%
● Refer to care pathway for further actions

Euglycemic DKA

● Partial treatment of DKA prior to admission with consequent lower blood glucose levels at
presentation

⇒ Treatment:
● Initiate glucose 105 straight away at 125ml/hr because the glucose is <14 mmol/L
● Begin with 0.1 units/kg/hr insulin rate
● If glucose falling despite 10% glucose reduces to 0.05 units/kg/hr to avoid hypoglycemia

→ Use of the sodium-glucose (SGLT) inhibitor class of drugs (e.g dapagliflozin, Canagliflozin,
Empagliflozin, Ertugliflozin, Sotagliflozin) increases the risk for Euglycemic DKA

Hyperosmolar hyperglycaemic state

→ Serum osmolarity = 2(Na + K) + urea + glucose (Normal range: 275-295 mOsm/kg)

⇒ Criteria:
1. Marked hyperglycaemia (glucose 30 mmol/L or more)
2. Hypovolaemia (High osmolarity triggering severe dehydration due to osmotic diuresis)
3. Osmolality> 320 mosmol/kg
4. Absence of significant ketones (ketones < 3 mmol/L) or acidosis (pH > 7.3 and bicarbonate >
15 mmol/L)

⇒ Clinical features:
● Polyuria, Polydipsia,
● Weakness, Weight loss,
● Tachycardia,
● Dry mucous membranes, Poor skin turgor,
● Hypotension, and, in severe cases, Shock.
● Acute cognitive impairment (lethargy, disorientation, stupor) (osmolalities > 330 mosmol/kg)
⇒ Management: The aim of treatment should be to replace approximately 50% of estimated fluid loss
within the first 12 hours and the remainder in the following 12 hours though this will in part be determined
by the initial severity, degree of renal impairment and co-morbidities such as heart failure, which may limit
the speed of correction.

● Fluid and Electrolytes: Similar to DKA → (IV) 0.9% NaCl solution as the principle fluid to
restore circulating volume and reverse dehydration.

● Monitoring: Osmolality and glucose: If fluid replacement is not causing the osmolarity and
glucose falling down, then we need to start insulin infusion. A fall in blood glucose of 5.5
mmol/L will result in a 2.4 mmol/L rise in sodium. Rising sodium is only a concern if the
osmolality is NOT declining concurrently.

● Insulin: @ 0.05 units/kg/hour indications-

1. >1 mmol/L 3 beta-hydroxybutyrate OR
2. <5 mmol/L/hr fall in glucose

● Prophylactic LMWH: Increased risk of thromboembolism

General principles: (FROM SUCCESS)

● A target blood glucose of between 10 and 15 mmol/L is a reasonable goal. Complete normalisation
of electrolytes and osmolality may take up to 72 hours.

● The patient should be encouraged to drink as soon as it is safe to do so and an accurate fluid
balance chart should be maintained until IV fluids are no longer required.

● Assessment for complications of treatment e.g. fluid overload, cerebral oedema or central pontine
myelinolysis (as indicated by a deteriorating conscious level) must be undertaken frequently (every
1-2 hours).

● Underlying precipitants must be identified and treated. An infective source should be sought on
clinical history and examination and C-reactive protein may be helpful.

● All patients should be assumed to be at high risk of foot ulceration if obtunded or uncooperative -
the heels should be appropriately protected and daily foot checks undertaken

⇒ Complications:
● Hypothermia
● Myocardial infarction
● Stroke
● Peripheral arterial thrombosis
● Seizures
● Cerebral oedema
● Central pontine myelinolysis (CPM)
● Venous thromboembolism
● Foot ulceration
Hypoglycaemia
⇒ Causes:
● Mismatch between insulin or oral hypoglycaemic agent and ingested calories or exercise
● Exogenous drugs
● Pituitary insufficiency
● Liver failure
● Addison’s disease
● Islet cell tumours
● Nonpancreatic insulin-secreting tumours
● Autonomic symptoms: Sweating, Palpitations, Shaking, Hunger, Nausea
● Neurological symptoms: Irritability, Confusion, Drowsiness, Odd behaviour, inco-ordination,
Speech difficulties, Focal neurological deficits, Seizures
→ Cognitive function deteriorates at levels <3 mmol/lL but Symptoms are uncommon > 2.5 mmol/L

⇒ Investigation
● Blood glucose
● Serum potassium level and ECG: Low K
● Liver function tests
● Urea and creatinine

⇒ Management
● Normal GCS: Oral Correction-

1. Fast-acting CHO (Glucogel under the tongue)

2. Followed by a long-acting CHO (e.g. biscuits or toast

● Low GCS: IV correction

1. Intravenous 10% glucose should be given in 50-ml boluses → (Check RBS after 10
mins)Reat Glucose bolus till blood glucose is in normal range.
2. When IV line is not accessible / Aggressive pt/ Having seizures:
Glucagon 1 mg IM (Don’t give in sulphonylurea drugs OD, Liver failure)
3. Admit sulphonylurea drugs or long-acting insulin continue 10%D @ 100ml/hr (Because they
have the chance of having recurrent hypoglycemia, need to start IV glucose.
4. Octreotide: Recurrent hypoglycemia due to Sulphonylurea OD, CKD
→ Recheck Glucose levels after 15 mins
Hypoglycaemia - pediatric
→ Capillary glucose levels are not accurate when it is < 3 mmol/L. That is why, Blood glucose levels are
preferred in asymptomatic pts to check hypoglycemia.

→ We start hypoglycemia correction if glucose is <2.6 mmol/L. Re-check blood glucose levels after 10mins

Normal GCS:
● <1yr: Milk feed
● >1yr: Fast-acting CHO (GlucoGel)

Low GCS:
● 1 mg glucagon >25 kg and 0.5 mg glucagon <25 kg
● Intravenous 10% glucose (2ml/kg) to a maximum dose of 5 ml/kg

Newly diagnosed diabetes mellitus

⇒ Criteria of diagnosis: Diabetes symptoms + RBS >11mmol/L

⇒ Treatment: If no complications, Refer to GP regardless the RBS. No treatment in ED

Adrenal gland

● G: Mineralocorticoids
● F: Glucocorticoids
● R: Androgen

Adrenal crisis (adrenocortical insufficiency)

⇒ General Causes: All are stress related
● Infection
● Trauma
● Myocardial infarction
● Stroke
● Asthma
● Hypothermia
● Alcohol
● Exogenous steroid withdrawal/reduction (Commonest)
● Autoimmune adrenalitis (Addison's disease)
⇒ Profoundly shocked: Tachycardic, Hypotensive, Vasoconstricted, Oliguric. Even with IVF, pt will not
improve. Other findings -
1. Hyponatremia
2. Hypotension
3. Hypoglycemia

4. Hyperkalemia
5. Hypercalcemia
6. Hyperpigmentation

→ Metabolic acidosis + Normal anion gap

⇒ Treatment: Hydrocortisone is preferred. Need to remember HC.

Primary hyperaldosteronism/Conn's syndrome/ b/l Idiopathic adrenal hyperplasia

⇒ Clinical features: Opposite to Adrenal crisis. (Diagnosis is more important than the treatment)
1. Hypokalemia
2. Hypernatremia
3. Controlled hypertension

⇒ Treatment: Spironolactone therapy for 4-6 weeks followed by surgical resection

→ Renal artery stenosis: similar symptoms + renal failure

Pheochromocytoma
⇒ Clinical features: HTN + Episodic Headache
● Hypertension
● Palpitations
● Sweating
● Pallor
● Headache
● Anxiety
● Pulmonary oedema
● Nausea and vomiting
● Altered level of consciousness

⇒ Investigations:
● Plasma Metanephrine Assay (Most sensitive)
● CT abdomen
→ ED investigations should look for evidence of hypertensive end-organ damage

⇒ Treatment:
● Blood pressure control is the mainstay of ED management.
● Phenoxybenzamine (α-blocker, non-competitive antagonism): 10-40 mg over one hour
(DOC)
● Phentolamine – competitive antagonism (Also an α-blocker)
● α-blockade precedes β-blockade (Labetalol)

Nelson's Syndrome

⇒ M/A:
● B/L adrenal gland removal for Cushing's syndrome → 10 -15 yrs of Negative feedback →
Continuous accumulation of ACTH → Pituitary adenoma → Very High ACTH/MSH →
Enlarged Pituitary adenoma will compress the Optic tract → B/L hemianopsia

⇒ Signs:
● Bitemporal hemianopsia
● Hyperpigmentation
● High prolactin
Hyperthyroid

⇒ Causes:
● Autoimmune:
➔ Graves Disease: Women aged 30-50 yrs. Antibodies against TSH- receptors cause diffuse
thyroid enlargement (Goitre). Associated with other autoimmune conditions such as Type-1
Diabetes and Pernicious anaemia. (Commonest cause)

➔ Hashimoto’s thyroiditis

● Drug-induced:
➔ Drug-induced hyperthyroidism: Occurs after the administration of either supplemental
iodine to those with prior iodine deficiency or pharmacologic doses of iodine (e.g Contrast
media, Medications) in those with an underlying nodular goitre.

➔ Amiodarone

● Infectious:
➔ Subacute thyroiditis
➔ Suppurative thyroiditis (Bacterial)

● Idiopathic
➔ Toxic nodular goitre (Second most common cause)

● Iatrogenic
➔ Thyrotoxicosis factitia: High quantities of exogenous thyroid hormone are consumed,
➔ Single manipulation

● Malignancy
➔ Toxic adenoma: is a single, hyperfunctioning nodule within a normally functioning thyroid
gland,
➔ Thyrotropin-producing pituitary tumours (Rare)

Thyroid storm

⇒ Causes:
⇒ Scoring system for thyroid crisis by Burch and Wartofsky (Not important for exam or ward)
1. Temperature
2. Cardiovascular Dysfunction
3. Central Nervous System Effects
4. Gastrointestinal effects
5. Precipitant history

⇒ Management:

● ABCD
● Inhibition of peripheral effects of thyroid hormone (Blocks T4 → T3 conversion)
1. Beta-blockers, Propranolol 60-80 mg PO
2. Hydrocortisone 200 mg IV OR Dexamethasone 2 mg IV

● Inhibition of thyroid hormone synthesis and release

1. Antithyroid treatment: Propylthiouracil and Carbimazole
2. Iodide

● Treat the underlying cause:

→ Aspirin should be avoided in a thyroid storm because it displaces Thyroxine from thyroid-binding
globulin

→ Other Beta-blockers to use: (Not imp)

● Propranolol 1 mg IV over 1 minute; if necessary repeat at 5-minute intervals, max total dose
10 mg
OR
● Esmolol is usually within the range 50-200 micrograms/kg IV loading dose
OR
● Metoprolol up to 5 mg at a rate 1–2 mg/minute, repeated after 5 minutes if necessary, Total
dose 10-15 mg
OR
● Verapamil 5-10 mg over at least 2 min IV

Myxoedema coma (Opposite to the Thyroid storm)

⇒ Clinical features:
1. Altered mental state ranging from poor cognitive function to coma
2. Hypothermia or the absence of fever despite severe infection
3. The presence of a precipitating event

⇒ Treatment:
● Thyroid hormone replacement
● Hydrocortisone 100 mg IV (Mainstay)
● Treat the underlying precipitant
● Supportive therapy
Pituitary apoplexy
→ Acute haemorrhage or infarction of the pituitary gland

⇒ Causes:
1. Head trauma.
2. Anticoagulation.
3. Pituitary radiotherapy.
4. Endocrine stimulation tests.
5. Sheehan’s syndrome

⇒ Clinical Features:
● Severe headache.
● Nausea, vomiting.
● Photophobia.
● Loss of consciousness.
● Meningism.
● Visual field defect

⇒ Investigations:
● Urgent MRI (No CT)
● ACTH, TSH, FSH, LH, and prolactin

⇒ Treatment:
● Supportive therapy (ABCDE)
● Hydrocortisone 100 mg intravenously
● Urgent neurosurgical opinion

***Shehan’s Syndrome: Sheehan syndrome occurs when the anterior pituitary gland is damaged due to
significant blood loss. Classically, this happens after delivery, in which the mother loses a significant amount
of blood. This blood loss results in the pituitary gland being infarcted and not being able to produce
hormones.

Diabetes insipidus
→ Impaired water resorption by the kidney

1. Cranial DI: 2. Nephrogenic DI:

(1st 2 cause****)

⇒ Investigation:
● Plasma osmolality: High
● Urine osmolality: Low
● Serum sodium: High
● Check serum potassium and calcium as potential causes
 ● CT head if a cranial cause is suspected
● Measure the pituitary function (TSH, ACTH, LH, FSH, Prolactin)
● Water deprivation test
● ADH stimulation test (To differentiate between Cranial and Nephrogenic DI)

⇒ Treatment:
● Cranial DI—desmopressin 1 mcg intranasally
● Nephrogenic DI—treat the cause
● Rehydrate—Match input to fluid losses and aim to reduce the serum sodium gradually

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

➔ Excess ADH → Water retention by the kidneys → Dilutional Hyponatraemia (Pt will be Euvolemic)
➔ Urine Sodium >20 mmol/L and Osmolality >500 mosm/kg

⇒ Causes:
● Central nervous system (CNS): Meningitis, Encephalitis, Abscess, Stroke, SAH, SDH, Head injury
● Malignancy: SMLC, Pancreatic cancer, Prostate cancer, Lymphoma
● Respiratory: Pneumonia, Aspergillosis
● Metabolic: Porphyria
● Drugs: Opiates, Psychotropics
● Trauma

⇒ Management:
● Treat the underlying cause
● Asymptomatic/ Mild- Moderate symptoms: Fluid restriction
● Severe Symptomatic(Seizures or Coma): Hypertonic saline +/- vasopressin
● Demeclocycline (Rarely used)
● Urgent review by a renal consultant

Ovarian Hyperstimulation Syndrome ******

→ Women with ovarian hyperstimulation syndrome (OHSS) will have recently had gonadotropin stimulation
to induce ovulation

⇒ Clinical features:

● Shortness of breath
● Abdominal discomfort
● GI disturbances
● Oliguria
● Peripheral oedema
● Lethargy
● Rapid weight gain

⇒ Investigations: ****

● CBC: Decreased Intravascular volume leads to Hemoconcentration and an increased Hct

● Coagulation profile: Hypercoagulable state
● Leukocyte count: A count higher than 2200 cells/micro-litre is related to the seriousness of
OHSS and predictive of thromboembolism. (Not due to any infection, so NO antibiotics)
● LFT
● RFT/electrolytes

⇒ Treatment:

● Maintenance of a high degree of clinical suspicion and a low threshold for admission
● Early surgical intervention in cases of ovarian torsion or haemorrhage
● Paracentesis to address ascites: This decreases pressure on the IVC and the diaphragm.
● Placement of a transthoracic tube to manage pleural effusions