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.
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
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
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.
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.
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.
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
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
47.
48.
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
Notas del editor
Most serious acute complications.
- High mortality rate if unrecognised.
- The overall mortality is <1%, mortality rate >5% in the elderly.
High-dependency unit (HDU)admission and insertion of central line in the following circumstances:
Elderly
Pregnant ladies
Heart or kidney failure
Other serious comorbidities
Severe DKA
Bicarb not indicated in DKA d/t :
Could l/t rise in PCO2 in CSF -> CSF Acidosis
Delay in fall of ketone bodies and lactate level
Risk of cerebral oedema especially in younger age group
Higher mortality and vascular complication than DKA
Progresses over days dehydration and metabolic disturbances more extreme
Once hypoglycaemia has been reversed, the patient should have the usual meal or snack that is due at that time of the day to prevent repeated hypoglycaemia
In chronic primary adrenal insufficiency, when patients experience serious infection or other acute major stress. Adrenal crisis may be the initial presentation in a previously undiagnosed patient, in whom the stressor appears to tip the balance to frank hypotension [1,8].
●It may also occur in patients with known primary or secondary adrenal insufficiency who are under-replaced, either because of: 1) insufficient daily doses of glucocorticoid and/or mineralocorticoid; 2) failure to take more glucocorticoid during an infection or other major illness; or 3) persistent vomiting or diarrhea caused by viral gastroenteritis or other gastrointestinal disorders, leading to decreased absorption.
The predominant manifestation of adrenal crisis is shock, but the patients often have nonspecific symptoms such as anorexia, nausea, vomiting, abdominal pain, weakness, fatigue, lethargy, fever, confusion, or coma (table 1).
Glucocorticoid deficiency can contribute to hypotension by causing decreased vascular responsiveness to angiotensin II and norepinephrine, decreased synthesis of renin substrate, and increased prostacyclin production
In the past, thyroid storm was commonly observed during thyroid surgery, especially in older children and adults, but improved preoperative management has markedly decreased the incidence of this complication. Today, thyroid storm occurs more commonly as a medical crisis rather than a surgical crisis.