2. 1. DIABETIC KETOACIDOSIS
• Is a metabolic emergency due to insulin
deficiency in which hyperglycemia is
associated with metabolic acidosis (D/t excess
ketones in blood)
3. Clinical Features
• Pt is usually a known case of Diabetes
• Complains of mental confusion, drowsiness, stupor or
coma
• Abdominal Pain is a dominant symptom
• Fruity odor in breath
• Kussmaul breathing to compensate for metabolic
acidosis
• May present with – polydypsia, polyuria and
dehydration(hypotension and oliguria)
• May present with anorexia, N&V and acute abdominal
pain (may be due to acidosis)
4. Investigations
• Urine examination shows glucose and ketones
• Plasma glucose raised >250mg
• Plasma ketone > 5mmol/l
• Urea, creatinine may be increased (urea in dehydrated
pt, creatinine in pt with diabetic nephropathy)
• Plasma electrolytes (sodium and potassium)
• CXR to r/o chest infections and ARDS (stress can cause
to ppt. DKA)
• ECG to rule out arrythmia due to hypokalemia
• ABG to confirm metabolic acidosis
6. • Bicarbonate therapy
– Indicated only in pt with severe acidosis especially
if hypotension is present
– Bicarbonate be given as infusion of isotonic
sodium bicarbonate (1.4%)
– Infusion to be stopped when the pH reaches 7.2
7. 2. HYPEROSMOLAR
HYPERGLYCEMIC STATE (HHS)
• Severe metabolic disorder in type-II DM, in
which uncontrolled hyperglycemia leads to
hyperosmolar state causing profound
dehydration and altered mental status
• Biochemical hallmark of HHS is extreme
hyperglycemia (as high as 2400mg/dl) in absence of
significant ketoacidosis
8. Clinical Features
• KCO type 2 DM and present with complaints of feeling unwell
with increased thirst, polyuria, confusion, drowsiness or
coma
• Hx of preceding illness for few days such as fever, vomiting or
gastroenteritis may be present which may lead to
dehydration (features of dry mouth, decreased skin turgor
and hypotension)
• Though dehydrated they may have polyuria from osmotic
diuresis due to severe hyperglycemia
• AKI may occur due to severe dehydration and hypovolemia
9. Investigations
• Blood sugar (markedly elevated ~ 600-2400mg/dl)
• Serum electrolytes – hypernatremia
• Blood urea may be raised
• Urine for sugar protein and microscopic examination
• CBC, Hb, TC, DC, ESR
• CXR to rule out infection
• Arterial Blood gases, pH, plasma bicarbonates to
distinguish from DKA
• ECG to rule out MI
10. MANAGEMENT
1. Immediate management in comatose pts
– Ensure adequate respiration- clear airway, place an
oropharyngeal airway
– Maintain circulation iv acess and NS drip
– Proper posture and care of bladder
2. Specific treatment of HHS
a. Fluid Replacement
Average fluid deficit is about 10L and should be corrected
intravenously.
Initially 2-3L of isotonic saline (0.9%) should be given over
Subsequently half strength (0.45%) saline should be used
Once the plasma glucose approaches 300mg/dl, 5%
dextrose-saline solution should be used
11. b. Insulin therapy
Regular insulin should be given as a low dose iv
infusion. The goal is to keep the plasma glucose
around 200 mg/dl
c. Potassium supplementation
d. Lactic Acidosis treated with iv sodium bicarbonate
e. Treatment of precipitating causes
12. 3. HYPOGLYCEMIA
Clinical Features
• can be classified in 2 main categories
– Adrenergic symptoms: sweating, tremor,
tachycardia, anxiety and hunger
– CNS dysfunction: dizziness, headache, clouding of
vision, loss of fine motor skills, confusion,
abnormal behavior, convulsion and Loss of
consciousness
13. Investigations
• Plasma glucose estimation
• Plasma electrolytes
• Liver function tests
• BUN, creatinine
• Serum cortisol
• USG abdomen (islet cell tumor and to r/o
other pathology)
14. MANAGEMENT
• Confirm diagnosis plasma glucose <40mg/dl
• Stop insulin and oral hypoglycemic drugs
• If patient is conscious – oral glucose intake
• If patient is unconscious- iv dextrose (50ml of
50% dextrose over 1 min) then maintain 10%
glucose infusion at a rate of 1-2ml/min until
the patient is fully conscious and able to take
glucose orally
15. 4. THYROID STORM
• Life threatening hypermetabolic state induced by
excessive release of thyroid hormones
• Dx is usually clinical & no specific tests are available
• Clinical syndrome caused by excess thyroid hormone
in the circulation and characterized by triad of
hyperpyrexia, tachycardia and agitation
HYPERPYREXIA
TACHYCARDIA AGITATION
16. Causes
• Grave’s disease
• Toxic multinodular
goiter
• Solitary toxic nodule
• Drugs – Amiadarone
Precipitating factor
• Sepsis/ surgery
• Abrupt withdrawl of
antithyroid drugs
• Thryroid surgery in ill
prepared patient
• Amiodarone
administration
17. Clinical features
• Agitation, restlessness, palpitation and
hyperpyrexia with temperature > 104 0F
• Thyroid enlargement, exopthalmos, lid lag,
profuse sweating, moist hands, tremor, thyroid
bruit and sinus tachycardia or atrial fibrillation
• Thyroid storm should be considered in patients
presenting with new onset tachycardia or atrial
fibrillation
• Protracted diarrhea may be presenting feature
18. Physical Findings
• Fever
• Excessive sweating
• CVS signs:
– Hypertension with wide pulse pressure
– Hypotension in later stages with shock
– Tachycardia disproportionate to fever
– Cardiac Arrythmias
• Neurologic Signs
– Agitation and confusion
– Hyperreflexia
– Tremors, seizures & Coma
• Signs of thyrotoxicosis
– Orbital signs /Goiter
19. Investigations
• TLC (reveals mild leukocytosis)
• Thyroid function tests T3↑ T4↑ TSH ↓ (confirmatory)
• Plasma electrolytes
• LFTs commonly reveal non specific abnormalities such
as raised AST, ALT, ALP & LDH
• BUN, creatinine
• EKG (to detect arrythmia)
• CXR – may reveal cardiac enlargement due to CHF; May
also reveal pulmonary edema caused by heart failure
and/or pulmonary infection
• Thyroid scan
20. MANAGEMENT
• Agitation: Diazepam (5-10mg iv)
• Hydaration maintain 3-5ltrs NS
• Atrial fibrillation: propranolol 1-5 mg iv or 40-
80 mg per oral
• Hyperpyrexia with cold sponges, fan or cooling
blankets. Not to use SALICYLATES as it cause
peripheral deiodination of T4 to T3
21. • Antithyroid Drugs
– Neomercazole: 20mg 8 hrly or propylthiouracil
600-1200 mg/day orally
• Iodine preparation
– Only after 1 hr of loading dose of neomercazole
– Sodium iopodate 500mg oraly/day
• Hydrocortisone 100 mg iv 6 hrly or
dexamethasone 2mg 6hrly
• TREATMENT OF PRECIPITATING CAUSE
22. 5. MYXEDEMA COMA
• Is a state of severe hypothyroidism
manifesting with coma and hypothermia
• Most commonly in older women with long
standing undiagnosed or undertreated
hypothyroidism who experience a significant
stress conditions like infection, systemic
disease, certain medication and exposure to a
cold climate
23. Clinical Features
• Usually present with stupor or coma, hypothermia or
hypoventillation
• History of thyroidectomy, radioactive treatment for thyrotoxicosis
or hypothyroidism may be present.
• Features of myxedema: pale, expressionless face, periorbital
edema, coarse dry skin, loss of hair and eyebrows, bradycardia,
Hypotension and delayed or absent tendon reflexes
• Neuropsychiatric manifestations: pyschosis with delusions &
hallucinations (myxedema madness), progressing to depressed
level of consciousness, convulsions and coma (myxedema coma)
• May present with hyponatremia or hypoglycemia
24. Investigation
• T3↓ T4 ↓ TSH ↑
• Blood sugar hypoglycemia
• Plasma electrolytes hyponatremia
• ABG for hypoxia
• ECG low voltage prolonged QT, inverted T
wave and J point elevation
• CXR may show cardiomegaly due to
pericardial effusion
25. MANAGEMENT
• Re-warm the patient by wrapping the patient
and raising room temperature BUT avoid
direct heat as it causes vasodilation and may
cause HYPOTENSION
• THYROXINE REPLACEMENT:
– Administer liothyronine (triiodothyronine or T3)
20μg 8 hourly for 24 hours. It is followed with oral
thyroxine 50 μg/day orally or via NG tube
26. • OTHERs
– Hypoglycemia is treated with 10% glucose infusion
– Dilutional hyponatremia is treated with fluid
restriction but if Na < 120mmol/L hypertonic
saline drip must be started
– Hydrocortisone 100 mg iv 6 hrly if concomittant
adrenal insufficiency
– Infection: antibiotics
27. 6. ACUTE ADRENAL CRISIS
• Sudden decline of adrenal cortical function
characterized by shock
28. Causes
• Sudden withdrawl of glucocorticoid /
mineralocorticoids in patients with Addison’s
disease or those receiving steroids for other
indication
• Sepsis, surgery or stress may precipitate acute
crisis in undiagnosed adrenal insufficiency
• Meningococcal septicemia with b/l adrenal
hemorrhage
• Anticoagulant therapy or coagulation disorder
may coz bilateral adrenal hemorrhage
29. Clinical Features
• Usu present in shock with sever HPN, cold clammy skin and
oliguria
• May also present with fever, anorexia, vomitting, muscle
cramps and abdominal pain (may simulate acute abdomen)
• SHOULD be suspected in all patients that present with
persistent HPN following surgery or infection, especially
when HPN doesn’t respond to fluid challenge and
vasopressor therapy
• Pateints also present with sypmptom related to associated
hyponatremia, hyperkalemia and hypoglycemia
30. Investigations
• Serum cortisol assay
– Normal value at 8AM is >100nmol/L, less than <100 nmol/L is
suggestive of adrenal deficiency
• Blood sugar is decreased
• Blood urea is raised
• Serum electrolyte Na↓ K ↑
• ACTH test (diagnostic): determine baseline serum cortisol
level, then administer ACTH 250mcg iv and then measure
serum cortisol 30 and 60 minutes after ACTH
administration. An increase of less than 9 mcg/dl is
considered diagnostic of adrenal insufficiency
• CT scan of adrenal gland (may show hemorrhage in the
adrenals or features of adrenal TB)
33. Prevention of Acute Adrenal
Insufficiency
• Double the doses of steroids in any intercurrent
infections
• Give parentral hydrocortisone in gastroenteritis
• Hydrocortisone before and during surgery in
patients known to have adrenal insufficiency
– Minor surgery: hydrocortisone 100mg i.m.
– Major surgery: hydrocortisone 100mg iv 6 hrly for
24 hrs then 50mg 6 hrly
34. References
• Davidson’s Principles and Practice of Medicine
• Harrison's Principles of Internal Medicine
• Medical Emergencies, Gopal Pd Acharya
