1. Myxedema coma is a life-threatening complication of severe untreated hypothyroidism, often precipitated by an acute illness. It involves altered mental status and multiple organ dysfunction. 2. Clinical features include symptoms of hypothyroidism along with hypothermia, hypotension, hypoventilation, coma and signs of precipitating illnesses. Investigations show features of hypothyroidism. 3. Treatment involves intensive care support including ventilatory support, cardiac monitoring and gradual rewarming. Thyroid hormone replacement is given cautiously along with treating any underlying illnesses.

1. ENDOCRINE
EMERGENCIES

2. 1. DIABETIC
KETOACIDOSIS

3. PRECIPITATING FACTORS:
DKA
Infection
Missed therapy
Acute coronary
syndrome
Cerebrovascular
Accident (CVA)
Surgery

4. PATHOPHYSIOLOGY

5. SIGN &
SYMPTOMS
Vomiting
Abdominal
pain
Dehydration
PolyurIa
Polydipsia
Lethargy
Deep
breathing
(Kussmaul)
Gradual
drowsiness

6. Diagnostic criteria (All three must be met) :
1. Capillary blood glucose >11 mmol/L
2. Capillary ketones >3 mmol/L or urine ketones ≥2+
3. Venous pH <7.3 and/or bicarbonate <15mmol/L
Severe DKA (≥1 of the following, consider admission to
HDU/ICU) :
1. Venous bicarbonate <5mmol/L
2. Blood ketones >6 mmol/L
3. Venous Ph <7.1
4. Hypokalaemia on admission <3.5mmol/L
5. Glasgow coma scale <12
6. Oxygen saturation <92% on air (Assuming no resp failure)
7. Systolic BP <90mmHg
8. Pulse >100 or < 60 beats/minute
9. Anion gap above 16

7. MANAGEMENT OF DKA
Step 1 :
- Put 2 large bore cannulae
- Start 0.9% N.S according to patient’s SBP
Step 2 :
- Add 50u Actrapid to 50mL 0.9% N.S.
- Commence a fixed rate IV insulin infusion
(0.1u/kg/hr based on pt’s estimated weight)
Step 3 :
- Asses patient’s vital sign (BP, PR, Temp, RR, O2 Sats, GCS,
Hydrational status)
- Investigation (Capillary and venous blood glucose , ABG,
Blood & Urine ketone, BUSE, FBC, Blood cultures, MSU,
ECG* & CXR*) *if indicated

8. Fluid and Potassium Replacement
 If SBP <90 mmHg :
- Give 500mL of 0.9% N.S over
10-15 mins.
- Repeat if SBP remains <90
mmHg
- If BP fails to pick up, consider
colloids (e.g : Gelafundin)
- Once SBP >90 mmHg, give
1000mL for 60 mins
 If SBP >90mmHg
- Give 1000mL for first 60 mins
 Consider potassium
replacement in the second
litre of fluid
 IV Bicarbonate is not indicated

9. CONT Mx of DKA
Step 4 :
- Look for underlying precepitating factor
and treat accordingly
Step 5 :
- Reasses pt’s vitals (Blood glucose, blood or urine
ketone, pH and bicarbonate in ABG, Potassium level
at 60 mins, followed by 4-6 hourly)
Step 6 :
- Continue fluid replacement via infusion pump
- Aim for :
1. Ketone falls at least 0.5 mmol/L/hr or Bicarbonate
rise 3mmol/L/hr
2. Blood glucose falls 3mmol/L/hr
3. Maintain serum potassium in normal range

10. Step 7 :
- Make sure of response to treatment
- If not, check if the insulin infusion pump working or
connecting correctly
- If no problem with infusion pump, increase insulin 1u/hr
increment until target achieved
Step 8 :
- Avoid Hypoglycaemia
- Once the blood glucose falls to <14 mmol/L :
a) Switch fluid replacement to 5% Dextrose at
125mL/hr and reduce insulin rate to 0.05 u/kg/hr
OR
b) Swith to 10% Dextrose at 125 mL/hr with no change
in insuline rate
Step 9 :
- Once DKA resolved follow step in managing
resolution of DKA

12. HYPEROSMOLAR
HYPERGLYCEMIC STATE
A condition where there is a relative insulin deficiency to maintain normoglycemia
but adequate to prevent lipolysis & ketogenesis.

13. Glycosuria
Osmotic
diuresis
Dehydration
Loss of water
and electrolyte
Hyperosmolarity
Hyperglycemia
Decreaase
glucose uptake
+
Increase
gluconeogenesis
Insulin
resistance
PATHOPHYSIOLOGY

14. CLINICAL FEATURES
• Polyuria, polydipsia
• Declining consciousness
• Drowsiness, lethargy
• Severe dehydration
• Neurological deficit e.g. seizures, coma

15. Precipitating factors for HHS
are:
a) Infections and sepsis
b) Thrombotic stroke
c) Intracranial haemorrhage
d) Silent myocardial infarction
e) Pulmonary embolism
Management goals
• Normalise the osmolality
• Replace fluid and electrolyte
losses
• Normalise blood glucose
• Prevention of complications
Diagnostic Criteria of HHS:
• Hypovolaemia
• Marked hyperglycaemia (BG >30 mmol/L)
• Osmolality >320 mosmol/kg

17. Hypoglycaemia

18. Definition
• Low plasma glucose level (<4.0 mmol/L)
• Development of autonomic or neuroglycopenia syndrome in patient
treated with insulin or OADs which are reversed by caloric intake

19. Symptoms
Autonomic
• Trembling
• Palpitations
• Sweating
• Anxiety
• Hunger
• Nausea
• Tingling
Neuroglycopenic
• Difficulty concentrating
• Confusion
• Weakness
• Drowsiness
• Vision changes
• Difficulty speaking
• Headache
• Dizziness

20. Nocturnal hypoglycaemia
• This risk is higher especially in the elderly
• Both physiologic and behavioural defences against hypoglycaemia have been
shown to be further compromised during sleep.
• Manifestation:
- poor sleep quality
- vivid dreams or nightmares
- waking with chills or sweating
- morning headache
- chronic fatigue
- mood changes and
- nocturnal convulsions

21. Severity
Severity Descriptions
Mild Autonomic symptoms are present. The individual is
able to self-treat
Moderate Autonomic and neuroglycopenic symptoms are
present. The individual is able to self-treat
Severe Individual requires assistance of another person.
May become unconscious, plasma glucose is usually
less than 2.8 mmol/L

22. Hypoglycaemic Symptoms Based on Blood
Glucose Levels
Adapted from Kedia N. Treatment of severe diabetic hypoglycaemia with glucagon: an underutilized therapeutic
approach. Diabetes, metabolic syndrome and obesity: targets and therapy, 2011

23. Risk Factors
• Advancing age
• Severe cognitive impairment
• Poor health knowledge
• Increased A1c
• Hypoglycaemia unawareness
• Long standing insulin therapy
• Renal impairment
• Neuropathy

24. Treatment
Education
• Patients at high risk for severe hypoglycaemia should be informed of
their risk and counselled, along with their family members and
friends.
• Patients at risk of hypoglycaemia are discouraged from driving,
riding, cycling or operating heavy machineries, as these activities
may endanger oneself and the public.

25. Treatment
Aim of treatment:
• Detect and treat a low blood glucose level promptly.
• Eliminate the risk of injury to oneself and to relieve symptoms
quickly.
• Avoid overcorrection of hypoglycaemia especially in repeated cases
as this will lead to poor glycaemic control and weight gain.

26. Treatment
Severity Treatment
Mild –
moderate
• Ingest 15 grams of simple carbohydrate (e.g 1
table spoon of honey, ¾ cup of juice, 3 tea
spoon of table sugar)
• Repeat blood glucose after 15 minutes. If the
level at 15 minutes is still <4.0 mmol/L, another
15 grams of carbohydrate should be taken.

27. Treatment
Severity Treatment
Severe Conscious Individual
Ingest 20 grams of carbohydrate and the above steps are repeated
Unconscious individual
• Should be given 20–50 mL of D50% intravenously over 1–3
minutes.
• Outside the hospital setting, a tablespoon of honey should be
administered into the oral cavity

28. Treatment
• Patients receiving anti-diabetic agents that may cause hypoglycaemia
should be counselled about strategies for prevention, recognition and
treatment of hypoglycaemia.
• Individuals may need to have their insulin regimen adjusted
appropriately to lower their risk.

29. Adrenal Crisis
• Acute adrenal insufficiency
• Precipitated by : infection, trauma, surgery, missed medication
• Hypovolaemia, hypotension, shock, hypogylcaemia

31. Diagnostic Test
Short Synacthen Test
• Confirms presence of hypoadrenalism
• Does not differ primary or secondary causes
• Diagnostic test
• Procedure:
• Take blood sample for baseline plasma cortisol
• Inject 250ug synacthen(tetracosactide) im/iv
• Take serial blood samples after 30, 60 mins for plasma cortisol measurement
NORMAL:-
Plasma cortisol
oBaseline: >190nmol/L
oAfter synacthen: increment of >200nmol/L,
peak >550nmol/L

32. Treatment
• Emergency measure
• Establish IV access with large gauge needle
• Draw blood for immediate serum electrolyte and glucose and routine
measurement of plasma cortisol and ACTH. (do not wait for lab result)
• Infuse 2 to 3 liters of isotonic saline or 5 percent dextrose in isotonic saline as
quickly as possible. Frequent hemodynamic monitoring and measurement of
serum electrolytes should be performed to avoid iatrogenic fluid overload.
• Give 4 mg dexamethasone as intravenous bolus over one to five minutes and
every 12 hours thereafter. Dexamethasone is the drug of choice because it
does not interfere with the measurement of plasma cortisol. If
dexamethasone is unavailable, intravenous hydrocortisone, 100 mg
immediately and every six hours thereafter, may be used.
• Use supportive measures as needed.(for any electrolyte imbalance)

33. • Subacute measures after stabilization
• Continue intravenous isotonic saline at a slower rate for next 24 to 48 hours.
• Search for and treat possible infectious precipitating causes of the adrenal
crisis.
• Perform a short ACTH stimulation test to confirm the diagnosis of adrenal
insufficiency, if patient does not have known adrenal insufficiency.
• Determine the type of adrenal insufficiency and its cause if not already
known.
• Taper parenteral glucocorticoid over one to three days, if precipitating or
complicating illness permits, to oral glucocorticoid maintenance dose.
• Begin mineralocorticoid replacement with fludrocortisone, 0.1 mg by mouth
daily, when saline infusion is stopped.

34. THYROID
STORM
Mariam

35. Definition of thyroid storm
• also referred as thyrotoxic crisis
• acute, life-threatening, hypermetabolic state induced by excessive
release of thyroid hormones (THs) in individuals with thyrotoxicosis
• Diagnosis is primarily clinical
• Several factors may precipitate the progression of thyrotoxicosis to
thyroid storm.

36. Aetiology

37. Precipitating Events

38. Clinical Presentation
General symptoms
• High fever (hyperpyrexia)
• Profuse sweating
• Palpitation
• Poor feeding and weight loss
• Respiratory distress
• Fatigue
GI symptoms
• Nausea and vomiting
• Diarrhoea
• Abdominal pain
Neurologic symptoms
• Anxiety
• Altered behaviour
• Seizures
• Coma

39. Burch & Wartofsky
scoring system 1993

40. Laboratory Investigations
• Results of thyroid studies are usually consistent
with hyperthyroidism and are useful only if the patient has not been
previously diagnosed.
• Test results may not come back quickly and are usually unhelpful for
immediate management.
• TFT : High T3, T4 ; Low TSH level
• FBC : may reveal leukocytosis
• LFT : High AST, ALT
• ABG and urinalysis : to assess and monitor short term management

41. Management of thyroid storm
The immediate goals when treating thyroid storm are to decrease thyroid
hormone synthesis, prevent thyroid hormone release, decrease peripheral
action of circulating thyroid hormone to reduce heart rate and support the
circulation, and to treat the precipitating condition [Nayak and Burman,
2006]
1. Supportive care
• ABCDE
• Cardiac Monitor and IV access.
• Fluids, Maintenance of Electrolytes and Glucose. Cooling for hyperthermia.
• Find and treat the precipitating factor ; infection/MI
• Add antibiotics as infection is a known precipitant and hard to distinguish
in ED

42. • When treating thyroid storm, one should consider the five ‘Bs’:
1. Block synthesis (i.e. antithyroid drugs);
2. Block release (i.e. iodine);
3. Block T4 into T3 conversion (i.e. high-dose propylthiouracil [PTU],
propranolol, corticosteroid and, rarely, amiodarone);
4. Beta-blocker;
5. Block enterohepatic circulation (i.e. cholestyramine) because in
thyrotoxicosis, there is increased enterohepatic circulation of thyroid
hormone

43. Ther Adv Endocrinol Metab. 2010 Jun; 1(3): 139–145.
Endocrine and metabolic emergencies: thyroid storm

44. Myxedema Coma
Asila

45. Myxedema coma
• It is a decompensated state of hypothyroidism resulting from
severe and prolonged depletion of thyroid hormones leading
to altered mental status and clinical features related to
multiorgan dysfunction.
• Occur as a result of long standing undiagnosed or undertreated
hypothyroidism and usually precipitated by systemic illness.
• Can arise from any causes of hypothyroidism :
Chronic autoimmune thyroiditis
Thyroidectomy, underwent radioactive iodine therapy for
hyperthyroidism.
Rare causes : secondary hypothyroidism, medication such as
lithium and amiodarone.

46. • Precipitants:
Infection (Pneumonia, UTI)
Myocardial infarction, stroke
Trauma
• Clinical features :
Usually in elderly > 65 years old
Symptoms of hypothyroidsim : tiredness,lethargy,low mood, cold-
disliking, increase weight, constipation, menorrhagia, hoarse voice,
decrease memory/ cognition, dementia, myalgia, cramps, weakness
Signs of hypothyroidism : hypothermia, hypotension, bradycardia,
hypoventilation, hyporeflexia, hypoglycemia,
Mental status : confusion, seizures, psychosis, coma
Goitre, cyanosis, ascites +/- non pitting oedema (lids, hands,feet) +/-
pleural or pericardial effusion, round puffy face, ileus (absent bowel
sound) ,dry skin, thinning hair, ecchymoses , purpura
Clinical features of precipitating factors

49. • Investigations:
1. FBC – normocytic normochromic ( reduce production of EPO)
/macrocytic anemia (low folate absorption and pernicious anemia
due to ileus ), leucocytosis (infection)
2. RP and electrolytes –hyponatremia (due to increase ADH),
increase creatinine
3. TFT- T3 ,T4 (low) TSH (high-primary hypothyroidism, low-
secondaryhypothyroidism)
4. Random Cortisol level - may coexist with adrenal insufficiency
5. DXT- hypoglycemia
6. Septic workout ( blood and urine C&S)
7. Cardiac enzymes –MI
8. ABG- hypoventilation causing respiratory acidosis
9. ECG- bradycardia, prolonged QT interval , ST elevation/depression,
T wave inversion
10. Chest X-ray – pneumonia, signs of heart failure

50. • Treatment:
(Immediate management is required before confirming the
diagnosis of myedema coma due to high mortality rate)
1. Airway maintanence- ICU admission may be required for
ventilatory support and continous cardiac monitoring
2. Gradual rewarming with blankets. ( Do not warm pt rapidly
as it can cause peripheral vasodilation and shock- aim : ½
degree celcius /h)
3. Thyroid hormone replacement :
- Give T3 (liothyronine) 5-20 mcg/12 h IV slowly (cautious it
may precipitate IHD)
- Alternatives: Levothyroxine
4. Hydrocortisone 100 mg / 18 h IV- vital if secondary
hypothyroidism is suspected: no goitre, no previous
radioiodine, no previous thyroid surgery
5. Antibiotic : Co-amoxiclav 1.2 g/8h nIV –if suspected infection

51. 6. IV Dextrose 5-10 % - To correct hypoglycemia
7. Further treatment :
- Monitor : rectal temp, 02 saturation, BP
-T3 5-20 mcg/4-12 h IV until sustained improvement (2-3 days)
- Then, levothyroxine 50 mcg/24h PO.
-Hydrocortisone ( use until adrenal insufficiency is excluded) and
IV fluids as needed