• Diabetic ketoacidosis (DKA) is most common among patients

with type 1 diabetes mellitus and develops when insulin levels

are insufficient to meet the body’s basic metabolic requirements.
• DKA is the first manifestation of type 1 diabetes in a minority of
patients.
• Insulin deficiency can be absolute (eg, during lapses in the
administration of exogenous insulin) or relative (eg, when usual
insulin doses do not meet metabolic needs during physiologic
stress).
• DKA is less common in type 2 diabetes mellitus, but it may occur in
situations of unusual physiologic stress.
• Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which
sometimes occurs in obese patients, often of African (including African-
American or Afro-Caribbean) descent.
• Patients with ketosis-prone diabetes can have significant impairment of
beta cell function with hyperglycemia, and are therefore more likely to
develop DKA when significant hyperglycemia occurs.
Common physiologic stresses that can trigger DKA include
•Acute infection (particularlypneumonia and urinary tract
infection)
•Myocardial infarction
•Stroke
•Pancreatitis
•Pregnancy
•Trauma
Some drugs implicated in causing DKA include:
◦Corticosteroids
◦Thiazide diuretics
◦Sympathomimetics
◦Sodium-glucose co-transporter 2 (SGLT-2) inhibitors
Symptoms and signs of diabetic ketoacidosis include symptoms of
hyperglycemia:
- nausea
- vomiting
- particularly in children—abdominal pain.

Lethargy and somnolence are symptoms of more severe decompensation.

Patients may be hypotensive and tachycardic due to dehydration and acidosis.
They may breathe rapidly and deeply to compensate for acidemia (Kussmaul
respirations). They may also have fruity breath due to exhaled acetone.
Fever is not a sign of DKA itself and, if present, signifies underlying infection.
In the absence of timely treatment, DKA progresses to coma and death.
• Acute cerebral edema, a complication in about 1% of DKA patients,
occurs primarily in children and less often in adolescents and
young adults.
• Headache and fluctuating level of consciousness
• Respiratory arrest can be the initial manifestation in others.
• The cause may be related to too-rapid reductions in serum
osmolality or to brain ischemia. Most likely in children < 5 years
when DKA is the initial manifestation of diabetes mellitus. Children
with the highest BUN (blood urea nitrogen) levels and lowest PaCO2
at presentation appear to be at greatest risk.
 Diagnosis of DKA

▪Arterial pH
▪Serum ketones
▪Calculation of anion gap
In patients suspected of having diabetic ketoacidosis:
• serum electrolytes
• blood urea nitrogen (BUN) and creatinine
• glucose
• ketones
• osmolarity
• urine for ketones
• arterial blood gas measurement
• DKA is diagnosed by an arterial pH < 7.30 with an anion gap > 12
and serum ketones > 5 mEq/L in the presence of hyperglycemia.
• A presumptive diagnosis can be made when urine glucose and
ketones are strongly positive.

Other laboratory abnormalities: hyponatremia, elevated serum

creatinine, and elevated plasma osmolality.
 Treatment

▪IV 0.9% saline

▪Correction of hypokalemia
▪IV insulin (as long as serum potassium is ≥ 3.3 mEq/L [3.3 mmol/L])
▪Rarely IV sodium bicarbonate (if pH < 7 after 1 hour of treatment)
 Hyperosmolar Hyperglycemic State (HHS)

• Hyperosmolar hyperglycemic state (hyperglycemic hyperosmolar nonketotic coma)

is a complication of type 2 diabetes mellitus and has an estimated mortality rate of
up to 20%, which is significantly higher than the mortality for diabetic ketoacidosis
(currently < 1%).
• It usually develops after a period of symptomatic hyperglycemia in which fluid
intake is inadequate to prevent extreme dehydration due to the hyperglycemia-
induced osmotic diuresis.
Precipitating factors include:
• Acute infections and other medical conditions
• Drugs that impair glucose tolerance (glucocorticoids) or increase
fluid loss (diuretics)
• Nonadherence to diabetes treatment
Serum ketones are not present because the amounts of insulin present
in most patients with type 2 diabetes are adequate to suppress
ketogenesis.
Because symptoms of acidosis are not present, most patients endure a
significantly longer period of osmotic dehydration before presentation,
and thus -
plasma glucose (> 600 mg/dL [> 33.3 mmol/L]) and osmolality (> 320
mOsm/L) are typically much higher than in diabetic ketoacidosis.
 Symptoms and Signs of Hyperosmolar
Hyperglycemic State

The primary symptom of hyperosmolar hyperglycemic state is

altered consciousness varying from confusion or disorientation to
coma, usually as a result of extreme dehydration with or without
prerenal azotemia, hyperglycemia, and hyperosmolality.
Focal or generalized seizures and transient hemiplegia may occur.
 Diagnosis of Hyperosmolar Hyperglycemic State

•Blood glucose level

•Serum osmolarity

Generally, hyperosmolar hyperglycemic state is initially suspected when a

markedly elevated glucose level is found in a fingerstick specimen obtained in
the course of a workup of altered mental status.
Measurement of serum electrolytes, blood urea nitrogen (BUN)
and creatinine, glucose, ketones, and plasma osmolality should
be done.
Urine should be tested for ketones.
Serum potassium levels are usually normal, but sodium may be
low or high depending on volume deficits.
BUN and serum creatinine levels are markedly increased.
Arterial pH is usually > 7.3.
Treatment of Hyperosmolar Hyperglycemic State

•IV 0.9% saline

•Correction of any hypokalemia
•IV insulin (as long as serum potassium is ≥ 3.3 mEq/L [≥
3.3 mmol/L])

Target plasma glucose is between 250 and 300 mg/dL (13.9 to 16.7 mmol/L)
 Symptoms and Signs of Hypoglycemia
autonomic symptoms: sweating
nausea
warmth
anxiety
tremulousness
palpitations
hunger
paresthesias
insufficient glucose supply to the brain causes headache, blurred or
double vision, confusion, difficulty speaking, seizures, and coma.
• Autonomic symptoms begin at or beneath a plasma glucose level
of about 60 mg/dL (3.3 mmol/L)
• Central nervous system symptoms occur at or below a glucose
level of about 50 mg/dL (2.8 mmol/L).
Risk factors for hypoglycaemia include:
• Insulin-dependent diabetes
• Previous history of hypoglycaemic episodes or reduced hypoglycaemia
awareness
• Impaired renal function
• Cognitive dysfunction/dementia
• Alcohol misuse
• Profound starvation
• Increased exercise
• Food malabsorption issues (e.g. coeliac disease, bariatric surgery,
gastroenteritis)
 Diagnosis of Hypoglycemia

•Blood glucose level correlated with clinical findings

•Response to dextrose (or other sugar) administration
 Treatment of Hypoglycemia

•Oral sugar or IV dextrose

•Sometimes parenteral glucagon
 Thyroid storm

• Thyroid storm is an acute form of hyperthyroidism that results from untreated

or inadequately treated severe hyperthyroidism.
• It is rare, occurring in patients with Graves disease or toxic multinodular goiter
(a solitary toxic nodule is a less common cause and generally causes less
severe manifestations).
• It may be precipitated by infection, trauma, surgery, embolism, diabetic
ketoacidosis, or preeclampsia.
 Thyroid storm

• Thyroid storm causes abrupt florid symptoms of hyperthyroidism with one

or more of the following: fever, marked weakness and muscle wasting,
extreme restlessness with wide emotional swings, confusion, psychosis,
coma, nausea, vomiting, diarrhea, and hepatomegaly with mild jaundice.
• The patient may present with cardiovascular collapse and shock.
• Thyroid storm is a life-threatening emergency requiring prompt treatment.
 Thyroid storm

Clinical features of a thyroid storm may include:

• Palpitations
• Tachycardia (often greater than 140 beats per minute)
• Tremor
• Nausea and vomiting
• Abdominal pain
• Reduced level of consciousness
• Confusion/agitation
• Seizures
Burch-Wartofsky Point Scale for the Diagnosis of Thyroid Storm
 Treatment of Thyroid Storm

Propylthiouracil: 600 mg orally given before iodine, then 400 mg every 6 hours

Iodine: 5 drops saturated solution of potassium iodide orally 3 times a day

or
10 drops Lugol solution orally 3 times a day
or
1g sodium iodide slowly by intravenous drip over 24 hours

Propranolol: 40 mg orally 4 times a day

or
1 mg slowly intravenously every 4 hours (not to exceed 1 mg/min) under close monitoring
A repeat 1-mg dose given after 2 minutes, if needed, or esmolol

Intravenous dextrose solutions

Correction of dehydration and electrolyte imbalance

 Treatment of Thyroid Storm

Cooling blanket for hyperthermia

Antiarrhythmics (eg, calcium channel blockers, adenosine, beta-blockers) if necessary for atrial
fibrillation

Treatment of underlying disorder, such as infection

Corticosteroids: Hydrocortisone 100 mg intravenously every 8 hours

or
Dexamethasone 8 mg intravenously once a day

Definitive therapy after control of the crisis via ablation of the thyroid with iodine-131 or surgical
treatment
 Myxedema coma
• Myxedema coma is a life-threatening complication of hypothyroidism, usually
occurring in patients with a long history of hypothyroidism.
• Its characteristics include coma with extreme hypothermia (temperature 24° to
32.2° C), areflexia, seizures, and respiratory depression with carbon dioxide
retention.
• Severe hypothermia may be missed unless low-reading thermometers are used.
• Rapid diagnosis based on clinical judgment, history, and physical examination is
imperative, because death is likely without rapid treatment.
• Precipitating factors include illness, infection, trauma, drugs that suppress the
central nervous system, and exposure to cold.