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Diabetic Ketoacidosis
DKA is a life-threatening metabolic complication caused by an absence or
inadequate amount of insulin. Affecting mostly type 1 diabetics, it is
marked by three concurrent abnormalities: hyperglycemia, dehydration
and electrolyte loss, and metabolic acidosis.

Pathophysiology
DKA can be initiated by trauma or conditions such as new-onset diabetes,
heart failure, or stress. The body under stress → decrease in the amount
of insulin → reduction of glucose entering cells and increased glucose
production by the liver → hyperglycemia → liver attempting to get rid of
excess glucose by excreting glucose with water, Na+ and K+ → polyuria →
dehydration.
DKA can also be caused by a lack of insulin → increased breakdown of
fat → increased fatty acid and glycerol → fatty acids converted into
ketones → acidosis → increasing respiratory rate and abdominal pain,
and acetone breath.

Clinical Presentation
■ Hyperglycemia
■ Polyuria
■ Dehydration
■ Weakness
■ Headache
■ Polydipsia
■ Acetone or fruity breath
■ Poor appetite
■ Nausea and vomiting
■ Abdominal pain, usually generalized or epigastric
■ Rigid abdomen and irregular bowel sounds
■ Kussmaul’s respirations
■ Hypothermia
■ Tachycardia
■ Hypotension
■ Glycosuria

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■ Ketones in blood and urine
■ Metabolic acidosis: pH <7.3, bicarbonate <15 mmol/L, blood glucose
>14 mmol/L, and ketonuria

Diagnostic Tests
■ Electrocardiogram
■ Chest x-ray
■ Urinalysis (note presence of ketones)
■ CBC
■ Serum electrolytes, glucose and ketone levels, and blood urea nitrogen
■ Urine, sputum, and wound and blood cultures
■ Arterial blood gases (ABGs) and anion gap (8–16 mEq/L or 8–16 mmol/L
normal)
■ Plasma osmolarity
■ Cardiac enzymes
■ Amylase and lipase levels
Note: Serum and urine should be negative for ketones.

Management
■ Provide airway support.
■ Administer O2 (3–6 L via nasal cannula).
■ Monitor respiratory rate and rhythm and blood pH.
■ Monitor vital signs.
■ Assess for changes in mental status.
■ Assess for signs of hypokalemia.
■ Monitor serum glucose and ketone levels.
■ Provide insulin replacement (insulin drip).
■ Provide electrolyte replacement.
■ Provide fluid resuscitation and monitor intake and output.

Diabetes Insipidus
DI is a disease manifested by the excretion of a large volume of urine
caused by ineffective production of antidiuretic hormone (ADH) at the
posterior pituitary.

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Pathophysiology
The four types of DI include:
■ Central DI
■ No ADH secretion
■ Cause can be congenital or idiopathic:
• Tumors in the central nervous system
• Cerebrovascular disease or trauma
• Infection
• Granulomas
• Pregnancy
• Brain death
■ Nephrogenic DI
■ Secretion of ADH but no stimulation to the nephron’s collecting
tubules
■ Cause can be congenital or idiopathic:
• Obstruction that hinders normal urine excretion
• Chronic tubulointerstitial disease
• Medications
• Electrolyte imbalance
■ Dipsogenic DI
■ Caused by a defect or damage to the thirst mechanism in the hypo-
thalamus
■ Results in an abnormal increase in thirst with an increased fluid
intake that suppresses ADH secretion and increases urine output
■ Gestational DI
■ Occurs only during pregnancy

Clinical Presentation
■ Large volume of very diluted urine with a low specific gravity (volume
does not decrease even with restricted fluids)
■ Extreme thirst, especially for cold water and sometimes ice or ice
water
■ Craving for fluid
■ Dehydration
■ Symptoms of hypovolemic shock: Changes in level of consciousness
(LOC), tachycardia, tachypnea, and hypotension

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Diagnostic Tests
■ Fluid deprivation test
■ Desmopressin stimulation
■ ADH test
■ Plasma and urine osmolarity
■ Serum chemistries and electrolytes
■ Urinalysis
■ CT scan of head to detect cranial lesions

Management
■ Administer desmopressin; ineffective in nephrogenic DI.
■ Administer hydrochlorothiazide or indomethacin (Indocin) for nephro-
genic DI.
■ If surgery is needed, provide emotional support to patient and family.
■ Assess intake and output.
■ Monitor vital signs frequently.
■ Administer fluids as needed.

Adrenal Crisis
Acute crisis, also known as acute adrenal insufficiency, is a serious com-
plication of a dysfunctional adrenal gland causing difficulties producing
aldosterone and cortisol hormones.

Pathophysiology
Destruction of adrenal cortex → hindered secretion of aldosterone and
cortisol → Addison’s disease → hypoglycemia and hypovolemic shock.
Causes of adrenal crisis include:
■ Recently halted chronic corticosteroid therapy
■ Injury to or infection of the adrenal gland
■ Chronic adrenal insufficiency
■ Bilateral adrenalectomy
■ Medications that suppress adrenal hormones
■ Medications that enhance steroid metabolism
■ Sepsis

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Clinical Presentation
■ Serious weakness and fatigue
■ Hypoglycemia
■ Fever
■ Vomiting
■ Diarrhea
■ Altered mental status and confusion
■ Hypotension
■ Tachycardia
■ Dysrhythmias
■ Lack of response to vasopressors

Diagnostic Tests
■ Cosyntropin (ACTH) stimulation test
■ CT scan or ultrasound of the adrenal glands

Management
■ Assess vital signs.
■ Weigh daily.
■ Strictly monitor intake and output.
■ Monitor serum glucose levels frequently.
■ Administer IV fluids.
■ Administer cortisol replacement medications (hydrocortisone IV).
■ Insert nasogastric tube if vomiting.
■ Reorient and minimize stress.
■ Provide small frequent meals and nutritional supplements.

Thyroid Storm
Thyroid storm is a rare life-threatening complication of a severe form of
hyperthyroidism that is characterized by high fever, extreme tachycardia,
and altered mental status, and is precipitated by stress.

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Pathophysiology
Thyrotropin-releasing hormone (TRH) is released from the hypothalamus
after exposure to stress → the pituitary gland releasing thyroid-stimulating
hormone (TSH) → causes the release of thyroid hormone (T3 and T4) from
the thyroid gland → T3 active form of thyroid hormone → increased levels
of thyroid hormone leading to hyperthyroidism or thyrotoxicosis → if
precipitated by stress (surgery, infection, trauma, DKA, heart failure, pul-
monary embolism, toxemia of pregnancy, thyroid hormone ingestion,
radioiodine therapy, discontinuation of antithyroid), further increase in
serum TH → thyroid storm.

Clinical Presentation
■ High fever and hyperthermia
■ Severe tachycardia (>200 bpm) with heart failure and shock
■ Restlessness and agitation
■ Abdominal pain
■ Goiter
■ Nausea and vomiting
■ Nervousness
■ Tremor
■ Confusion
■ Delirium
■ Coma
Exaggerated symptoms of hyperthyroidism with disturbances of major
systems:
■ GI:
■ Weight loss
■ Diarrhea
■ Abdominal pain
■ CV:
■ Edema
■ Chest pain
■ Dyspnea
■ Palpitations

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Diagnostic Tests
■ Serum thyroid panel
■ Liver function tests

Management
“Triangle of Treatment”:
■ Decrease sympathetic outflow (beta blockers: esmolol–drug of
choice).
■ Decrease production of TH (propylthiouracil [PTU] or methimazole).
■ Decrease peripheral conversion of T4 to T3 (PTU, beta blockers, and
steroids).
■ Prevent cardiac collapse.
■ Administer humidified O2.
■ Monitor ABGs and provide continuous pulse oximetry monitoring.
■ Monitor vital signs frequently.
■ Administer IV fluids containing dextrose to replace liver glycogen.
■ Give beta blockers; if contraindicated, give calcium channel blockers
to prevent excessive hyperthermia.
■ Give acetaminophen; salicylates are contraindicated.
■ Monitor intake and output.

Syndrome of Inappropriate Antidiuretic Hormone

SIADH is the continuous production of ADH from the pituitary gland
despite low osmolarity. It is frequently manifested by hyponatremia.

Pathophysiology
Malignant tumors, disorders of CNS and medications → increased secre-
tion of ADH → hyponatremia → increased water retention → stimulation
of renin-angiotensin system → increased excretion of sodium in urine.

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Clinical Presentation
■ Concentrated urine
■ Water retention
■ Lethargy
■ Dilutional hyponatremia
■ Signs and symptoms of hyponatremia:
■ Poor skin turgor and dry mucosa
■ Headache
■ Decreased saliva
■ Orthostatic hypotension
■ Anorexia, nausea, and vomiting
■ Abdominal cramps
■ Irritability, confusion, and disorientation
■ Seizures

Diagnostic Tests
■ Comprehensive metabolic panel
■ Urine Na+ and electrolytes
■ Serum and urine osmolarity
■ Ultrasound of kidneys
■ CT scan of head

Management
■ Monitor intake and output.
■ Weigh daily.
■ Monitor for CNS changes.
■ Assess for edema of extremities.
■ Institute fluid restrictions.
■ Closely monitor electrolytes.
■ Administer demeclocycline (Declomycin, Declostatin, Ledermycin) to
treat hyponatremia by inhibiting the action of ADH.
■ Administer conivaptan (Vaprisol) to treat hyponatremia.
■ Provide emotional support.

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