ENDOCRINE EMERGENCIES

OUTLINE
• DEFINITION
• PATHOPHYSIOLOGY
• CAUSES
• COMPLICATIONS
• MANAGEMENT
 DIABETIC
KETOACIDOSIS
NURUL NAJIHA BINTI ZAINUDIN
012014100095
 HYPERGLYCEMIA
>11MMOL/L

More common in
Diabetes mellitus type
1

DKA
KETOSIS
KETONEMIA
ACIDOSIS
>3MMOL/L
KETONURIA >2+
 CAUSES OF DKA
• Non-compliance to insulin
• Infections
• Stroke, MI
• Pancreatitis
• Trauma
• Alcohol intake/ drug abuse
• Medications
 CLINICAL FEATURES
• Polydipsia
• Polyphagia
• Weight loss
• Abdominal pain
• Vomiting
• Leg cramp
• Visual disturbances
• Shortness of breath (Kussmaul breathing)
• Fruity smelling breath
• Confusion, drowsiness, coma
Sign of dehydration
- Sunken eyes
- Dry lips
- Coated tongue
- Tachycardia
- Tachypneoic
- CRT >2s
- Hypotension
 INVESTIGATIONS
Full blood count Increase WBC counts
Renal profile Elevated urea & creatinine
Hyponatremia, hypokalemia
Blood glucose level >11mmol/L
Arterial blood gas pH <7.3
HCO3 <15mmol/L
Blood ketone >3mmol/L
Urine ketone >2+
Blood culture, C-reactive protein Infection screening
Chest x-ray Sign of infection
ECG
Severity of DKA:
a) Mild (venous pH <7.3, bicarbonate <15)
b) Moderate (venous pH <7.2, bicarbonate <10)
c) Severe (venous pH <7.1, bicarbonate <5)
 TREATMENT
a) Correct hypovolemia/dehydration
- Average 6-8L may need to be given for first 24hr
- Normal saline 0.9%
- 1L in 1 hr
- 1L in 2 hr
- 1L in 4 hr
- 1L in 6 hr
- 1L in 8 hr
- Monitor patient closely and look out for fluid
overload or underhydration
b) Insulin therapy
- Continuous intravenous insulin infusion is
treatment of choice. Soluble insulin is diluted in
0.9% saline at a concentration of 1U/ml
- Give IV bolus 10U soluble insulin followed by
6U/hr by infusion pump
- Blood glucose should be monitored hourly
c) Potassium replacement
- Administration of potassium should begin:
- When ECG shows no evidence of hyperkalemia
- When ample urine output is demonstrated
- When plasma K is <5mmol/L
- Add 1g KCL in each 0.5litre of fluid initially
- Adjust according to serum potassium level:
Plasma potassium Potassium added
<3 40
3-4 30
4-5 20
>5 or renal failure none

- Do BUSE 4-6hrly and ECG monitoring

d) Bicarbonate therapy ( should be considered
after adequate fluid resuscitation when:
- Arterial pH <6.9
- Severe hyperkalemia with ECG changes
• A solution of 8.4% sodium bicarbonate mixed
with sterile water or 0.45% saline is preferred
than bolus infusion
e) Treat precipitating factors
ICU/HDU admission:
a) Elderly
b) Pregnant ladies
c) Heart or kidney failure
d) Severe DKA
e) GCS <12
f) Hypotension
 COMPLICATIONS OF DKA
• Cerebral edema (any neurological symptoms,
begin mannitol 1g/kg)
• Hypoglycemia
• Hypokalemia/hyperkalemia
• Pulmonary oedema
• What are the diagnostic features of DKA?

Blood glucose >11mmol/L

Acidosis pH <7.3 HCO3 <15mmol/L
Ketonemia/ ketonuria
What are the causes of DKA?

Stopping insulin / reducing the dose

New onset of DM
Stress (infection, trauma, MI, stroke)
• Goal of management?

Correct fluid loss

Correct electrolyte imbalances
Correct metabolic imbalances
Treat hyperglycemia
Treat precipitating factors
 REFERENCE
• Tintinalli’s Emergency Medicine 8th Edition
• CPG Management of Type 2 Diabetes Mellitus
5th Edition
• Sarawak Handbook of medical emergencies,
3rd edition
 HYPEROSMOLAR
HYPERGLYCEMIC STATE
(HHS) &
HYPOGLYCEMIA

NURUL SOLEHAH BINTI BAHARUDIN

012014100068
Definition of HHS
• Characterized by progressive hyperglycemia and
hyperosmolarity typically found in a debilitated
patient with poorly controlled or undiagnosed
T2DM, limited access to water and commonly a
precipitating illness
Diagnostic Criteria of HHS
• Severe hyperglycemia with serum glucose usually
>33.3mmol/L,
• an elevated calculated plasma osmolality of
>315mmol/kg,
• serum bicarbonate >15mmol/L
• arterial pH >7.3
• serum ketone - negative to mildly positive in 1:2
dilution
Pathophysiology
Causes
Clinical Features
HISTORY PE
• Elderly
• volume depletion
• undiagnosed/
uncontrolled T2DM • poor skin turgor
• changed mental status for • dry mucous membrane
days or weeks • sunken eyes
• weakness • hypotension
• anorexia
• normothermia/
• fatigue
hypothermia
• dyspnea
• chest pain • seizure (focal)
• abdominal pain
Investigations
• Plasma glucose
• FBC
• ABG/VBG
• Urinalysis
• Renal profile
• blood and urine culture
• ECG
• CXR
Management
Goals
• Replace fluid
• Correct electrolyte abnormalities
• Gradual correction of hyperglycemia and
osmolality
• Identify and treat precipitating cause
• Prevent of complications (frequent monitoring)
Principles of Treatment
• Start with IV fluid 1L normal saline per hour
• IV 0.45% saline is recommended if the osmolality is not
declining despite adequate positive fluid balance
• Monitor serum osmolality regularly to prevent harmful
rapid changes
• Sodium is expected to rise initially. Not indication for
hypotonic fluids. Rate of plasma sodium fall not exceed
10mmol/L in 24h
• Blood glucose fall </= 5mmol/L
• Low dose IV insulin (0.05u/kg/h) commenced once blood
glucose is no longer fall or immediately if there is
significant ketonemia
• Prophylactic low molecular weight heparin is
recommended unless contraindicated for 2-3d to
prevent thrombosis
• Hyperkalemia, hypokalemia, hypophosphatemia
and hypomagnesemia are common and should be
corrected accordingly
Complication
• Hypoglycemia
• Hypokalemia
• Pulmonary edema

due to overzealous resuscitation and inadequate

monitoring
HYPOGLYCEMIA
• Definition :- (Whipple's triad)
• symptoms consistent with hypoglycemia
• Low plasma glucose level (<4mmol/L in DM or
<2.7mmol/L)
• Symptoms resolve with glucose administration
Symptoms of Hypoglycemia

• Altered mental status

• Seizure
• Focal neurological
deficit
• Unresponsiveness
1. Fully conscious
Give 15-20g simple and complex carbohydrates (1-
2 tablets of glucose/sweets, 3 teaspoon of sugar, 1-
2 cups of milk, followed by 3 pieces of crackers or
1-2 pieces of bread)
Repeat the procedure if blood glucose still
<4mmol/L after 15 minutes
Ensure adequate subsequent food intake to
prevent relapse
2. Mental function is impaired
medical emergency : set IV line, turn pt to left
lateral position
IV 50% dextrose 25-50ml followed by saline flush.
Repeat every 10-15 minutes until mental function
recovers or blood glucose is normal, followed by
infusion of 5-10%DW or a glucose drink if pt regain
full consciousness
If due to overdose of long acting insulin or OAD,
10% dextrose drip should be continued for 24-48h
SC / IM Glucagon 1mg if IV access is difficult.
Advice pt to eat/drink (1) as glucagon lasts for 10-
15 min
Pt who remain uncoscious after prolonged
hypoglycemia may need to be given tx for cerebral
edema with IV dexamethasone 4mg 6hourly or IV
mannitol , or consider other causes of coma
(stroke, drug overdose)
What are the diagnostic criteria
for HHS?
• Severe hyperglycemia with serum glucose usually
>33.3mmol/L,
• an elevated calculated plasma osmolality of
>315mmol/kg,
• serum bicarbonate >15mmol/L
• arterial pH >7.3
• serum ketone - negative to mildly positive in 1:2
dilution
Complications of HHS?
• Hypoglycemia
• Hypokalemia
• Pulmonary edema
How to diagnose hypoglycemia
Whipple's triad
hypoglycemic symptoms
blood glucose <4mmol/L
symptoms resolve with administration of glucose
What are hypoglycemic
symptoms?
References
• Tintinallis Emergency Medicine 8th Edition
• Sarawak Handbook of Medical Emergency 3rd
Edition
• CPG
NNAME: SALINI BALAKRISHNAN
MATRIC NO.: 012015100112
 OUTLINES
 Physiology
 Definition
 Cause
 Pathophysiology
 Precipitants
 Clinical features
 Diagnostic criteria
 Investigations
 Treatment
 Complications
 Questions
PHYSIOLOGY
 PHYSIOLOGY
• Thyroid hormone production dependent on adequate iodine intake.
• Thyroid hormone is reversible bound to various proteins including
thyronine-binding globulin (TBG)
• Free unbound portions are biologically active
• T4 is the predominant circulating hormone
• T4 is deiodinated to T3
• T3 is biologically more active than T4 but has a shorter half-life
 DEFINITION
Hyperthyroidism = excess circulating hormone resulting only from
thyroid gland hyperfunction

Thyrotoxicosis = excess circulating thyroid hormone originating

from any cause (including thyroid hormone
overdose)
Thyroid storm =an acute, severe, life-threatening hypermetabolic state of
thyrotoxicosis caused either by excessive release of
thyroid hormones or altered peripheral response to thyroid
hormone following the presence of one or more precipitants
 CAUSE
- Graves’sdisease - caused by the thyrotrophin receptor antibodies that
stimulate excess and uncontrolled thyroidal synthesis and secretion of
thyroid hormones
- Occursmost frequently in young women (10 times more common in
women compared with men) at any age group
 PATHOPHYSIOLOGY
Starts with adrenergic hyperactivity either by increased release of thyroid
hormones (with/without increased synthesis) or increased receptor
sensitivity

Excess thyroid hormones cytoplasm stimulate changes

specific to the tissue sti

Precipitants will multiply the effect of thyroid hormones by freeing thyroid

hormones from their binding sites or increasing receptor sensitivity
PRECIPITANTS
CLINICAL FEATURES
DIAGNOSTIC CRITERIA
DIFFERENTIAL DIAGNOSIS
 INVESTIGATIONS
INVESTIGATIONS RATIONALE

Thyroid function test To confirm hyperthyroidism

Chest X-ray To rule out infection

Electrocardiogram Sinus tachycardia, atrial fibrillation

Premature ventricular contractions and heart blocks

Liver function test Raised liver enzymes

 TREATMENT

Treatment aims are as follows:

1. Supportive care
2. Inhibition of new hormone synthesis
3. Inhibition of thyroid hormone release
4. Peripheral ß-adrenergic receptor blockade
5. Preventing peripheral conversion of thyroxine to triidothyronine
 PREPARATION FOR SURGERY
• Some patients are to undergone emergency surgery
• However, some supplement are recommended to be taken prior to the
surgical procedures
• They are important as it may precipitate thyroid storm.
 COMPLICATIONS
• High output cardiac failure
• Cardiac arrhythmias
• Delirium, seizures, coma
 QUESTIONS
1. What should be given preoperatively to patients with severe thyrotoxicosis?
A. Radioactive iodine
B. Phentolamine
C. Lithium
D. Lugol’s iodine

2. Which of the following is not seen in thyroid storm?

A. Hyperthermia
B. Tachyarrhythmias
C. Confusion and hypomania
D. Left upper quadrant pain
 QUESTION
3.Which of the following is the best treatment of thyroid storm?
A. Fluid hydration, cooling blanket, and dopamine
B. Fluid hydration, cooling blanket, beta-blockers, propyl thiouracil,
corticosteroids, and, later, iodine
C. Hydration, antipyretics, beta blockers, and benzodiazepines
D. Hydration, antipyretics, and beta-blockers
 QUESTION
4. A patient is about to undergo thyroid surgery for hyperthyroidism and
develops a thyroid storm. Which one of the following is not appropriate
for this patient?
A. Beta-blocker
B. Propylthiouracil
C. Iodine solution
D. Aspirin
 QUESTION
5. A 48-year-old male with a past medical history of thyrotoxicosis and
medication non-adherence is seen at an outpatient clinic. He has not been
taking the prescribed methimazole for the last three weeks. He complains of
palpitations at rest, frequent loose bowel movements, nausea, hand tremors,
and diaphoresis. On examination his heart rate is 122/min, respiratory rate
is 26/min, the temperature is 103 degrees F, and BP 142/88. He does not
have proptosis or conjunctival erythema. He seems confused on multiple
occasions during the encounter. What do you expect to find in his lab
works?
A. Normal TSH, high FT4, hypercalcemia, low PTH, transaminitis
B. Low TSH, high FT4, hypercalcemia, high PTH, transaminitits
C. Low TSH, high FT4, hypocalcemia, high PTH, normal LFTs
D. High TSH, high FT4, hypocalcemia, Low PTH, normal LFTs
 REFERENCE
 Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9e.
Judith E. Tintinalli, J. Stephan
 ADRENAL
INSUFFICIENCY

SHAMALA ARUMUGAM
012014100176
Definition
• Known as addisons disease
• Life threatening condition due to insufficient
cortisol production

• Causes
- Autoimmune disease
- Removal or destruction of adrenal gland
- Infection
- tumours
Presenting history
• Non specific weakness
• Fatigue
• Weight loss
• GI upset (nausea, vomitting,
abdominal pain, diarrhea)
• Altered mental status
• Confusion
• Coma and lethargy
Clinical features
• Dehydration • Look for persistent
hypotension and
• Lethargy orthostatic
• Altered mental hypotension
status • Evidence of sepsos
• Cushingoid facies or trauma
• Hyperpigmentation
in buccal mucosa
Precipitating factors
• Stress
• Fever
• Recent surgery
• MI
• Trauma
• Drug history of long term steroid use
Investigation
• Haematological
- Full blood count
- renal profile
- ABG
- Plasma cortisol and ACTH

- Chest Xray
- ECG
- BLOOD CULTURE AND URINALYSIS
MANAGEMENT
• 1. Supportive measures
- Management in critical care
- Monitor ( ECG, Pulse oximetry, vital signs)
- 2 large bore IV access
- Secure airway, give supplemental oxygen & fluid administration
(0.9% NS)

2. Drug Therapy
- IV Dextrose 50% 40ml ( correct hypoglycaemia)
- Glucocorticoid replacement
- IV NaHCO3 (50mmol/L over 1 to 2 hrs) monitor acid base with
ABG
- TREAT PRECIPITATING CAUSE
CUSHING SYNDROME
CUSHING SYNDROME
• caused by high blood levels of cortisol
• Cushings disease is Cushings syndrome that results
from excess pituitary production of ACTH, usually
secondary to a pituitary adenoma
 AETIOLOGY
• Excess secretion of cortisol by the adrenal cortex can be
ACTH dependent or ACTH independent
• ACTH dependent hyperfunction may result from excess
secretion by the pituitary gland, ectopic secretion from
neoplasm
• ACTH independent hyperfunction usually results from
therapeutic administration of corticosteroids or from
adrenal neoplasms
• Be sure to rule out other conditions associated with
hypercortisolism such as pregnancy, depression, alcohol
dependence, poorly controlled diabetes mellitus
SIGN
• Moon facies with plethoric appearance,
• Truncal obesity with prominent supraclavicular
• Dorsal fat pads (buffalo humps)
• Muscle wasting and weakness
• Skin appears thin, poor wound healing, and
purple abdominal striae
• Females with adrenal tumours can also come
with hypertrichosis, temporal balding, hirsutism
and menstrual irregularities
 INVESTIGATIONS
• Dexamethasone suppression test: Low dose
dexamethasone test administration of 0.5mg
dexamethasone 6 hourly for 48 hours
(N: <50nmol/L)
• Urinary Free Cortisol (UFC) level
• Serum ACTH level (N: <4pmol/L)
• Pituitary imaging using MRI
with gadolinium
 TREATMENT

Medical treatment Surgical treatment

• Ketoconazole • Transphenoidal surgery
200mg/400mg TID
• Adrenalectomy
• Add
• Metyrapone 250mg TID
up to 4g/day
• Add
• Aminogletethimide
250mg TID
• Consider Mitotane
PHEOCHROMOCYTOMA
PHEOCHROMOCYTOMA
• Neuroendocrine tumor of medulla of adrenal
glands or extra-adrenal chromaffin tissue that
secretes excessive amounts of catecholamines
• May occur as single tumour or as more than one
growth
• Usually develops in medulla of one or both adrenal
glands
Sign and symptoms
• Hyperglycemia
• Tachycardia
• Anxiety
• Chest pain
• Palpitation
• Severe headache
• Flushing
• Diaphoresis
• Abdominal pain
• Increased appetite
• Weight loss
Investigations
• 24 hr urine sample
• Plasma levels of catecholamines
• Glucose test
• Adrenal biopsy
• Abdominal CT scan
• MRI of abdomen
• Ultrasonography
Treatment
• Pharmacologic therapy Before and during surgery
-decrease Bp
a) long acting alphablocker
(a)alpha- adrenergic blocking agents
-phentolamine -phenoxybenzamine
(b)smooth muscle relaxants b) ca channel blockers
-sodium nitroprusside
-nifedipine
c) Beta adrenergic blocking
agents
• Surgical therapy -propanolol
-adrenalectomy
d) cathecholamine synthetic
inhibitors
-methyrosine
Mcq : which is true regarding
adrenal insufficiency?
• Fatigue, weight loss and GI upset are the symptoms
• adrenal insufficiency is not a life threatening
condition
• Requires supportive care
• Autoimmune, anatomic destruction or removal of
gland, infections and tumours are causes of adrenal
insufficiency
• Is due to sodium retention
Mcq : which is true regarding
Cushing syndrome?
• caused by high blood levels of cortisol
• Truncal obesity is a feature
• there is decrease production of ACTH
• Adrenalectomy is not a surgical treatment for
Cushing syndrome
• Pituitary imaging using MRI with gadolinium is an
investigation
REFERENCE
• Tintinalli’s Emergency Medicine 8th Edition
• CPG Management of Type 2 Diabetes Mellitus 5th
Edition
• Sarawak Handbook of medical emergencies, 3rd
edition