Signs and symptoms

Excessive urination and extreme thirst (especially for cold water) are typical for DI. Symptoms of diabetes insipidus are quite similar to those of untreated diabetes mellitus, with the distinction that the urine is not sweet and there is no hyperglycemia (elevated blood glucose). Blurred vision is a rarity.

The extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating, weight gain, and growth as well. They may present with fever, vomiting, or diarrhea. Adults with untreated DI may remain healthy for decades as long as enough water is drunk to offset the urinary losses. However, there is a continuous risk of dehydration.

Diagnosis

In order to distinguish DI from other causes of excess urination, blood glucose, bicarbonate and calcium need to be tested. Electrolytes can show substantial derangement; hypernatremia (excess sodium levels) are common in severe cases. Urinalysis shows low electrolyte levels, and measurement of urine osmolarity (or specific gravity) is generally low.

A fluid deprivation test helps determine whether DI is caused by:

1. excessive intake of fluid

2. a defect in ADH production

3. a defect in the kidneys' response to ADH

This test measures changes in body weight, urine output, and urine composition when fluids are withheld. Sometimes measuring blood levels of ADH during this test is also necessary.

To distinguish between the main forms, desmopressin stimulation is also used; desmopressin can be taken by injection, a nasal spray, or a tablet. While taking desmopressin, a patient should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in central nervous system. If desmopressin reduces urine output and increases osmolarity, the pituitary production of ADH is deficient, and the kidney responds normally. If the DI is due to renal pathology, desmopressin does not change either urine output or osmolarity.

If central DI is suspected, testing of other hormones of the pituitary, as well as magnetic resonance imaging (MRI), is necessary to discover if a disease process (such as a prolactinoma, or histiocytosis, syphilis, tuberculosis or other tumor or granuloma) is affecting pituitary function.

Habit drinking (in its severest form termed psychogenic polydipsia) is the most common imitator of diabetes insipidus at all ages. While many adult cases in the medical literature are associated with mental disorders, most patients with habit polydipsia have no other detectable disease. The distinction is made during the water deprivation test, as some degree of urinary concentration above isosmolar is eventually obtained before the patient becomes dehydrated.

Treatment

Central DI and gestational DI respond to desmopressin. In dipsogenic DI, desmopressin is not usually an option. Desmopressin will be ineffective in nephrogenic DI. Instead, the diuretic hydrochlorothiazide (HCT or HCTZ) or indomethacin can improve NDI; HCT is sometimes combined with amiloride to prevent hypokalemia. Again, adequate hydration is importantant for patients with DI, as they may become dehydrated easily.

Lesson 10. HAEMATOLOGY EMERGENC ES

HEMORRHAGIC SHOCK

Shock is a state of inadequate perfusion, which does not sustain the physiologic needs of organ tissues. Many conditions, including blood loss but also including nonhemorrhagic states such as dehydration, sepsis, impaired autoregulation, obstruction, decreased myocardial function, and loss of autonomic tone, may produce shock or shocklike states.

Pathophysiology: In hemorrhagic shock, blood loss exceeds the body's ability to compensate and provide adequate tissue perfusion and oxygenation. This frequently is due to trauma, but it may be caused by spontaneous hemorrhage (eg, GI bleeding, childbirth), surgery, and other causes.

Most frequently, clinical hemorrhagic shock is caused by an acute bleeding episode with a discrete precipitating event. Less commonly, hemorrhagic shock may be seen in chronic conditions with subacute blood loss.

Physiologic compensation mechanisms for hemorrhage include initial peripheral and mesenteric vasoconstriction to shunt blood to the central circulation. This is then augmented by a progressive tachycardia. Invasive monitoring may reveal an increased cardiac index, increased oxygen delivery (ie, DO₂), and increased oxygen consumption (ie, VO₂) by tissues. Lactate levels, acid-base status, and other markers also may provide useful indicators of physiologic status. Age, medications, and comorbid factors all may affect a patient's response to hemorrhagic shock.

Failure of compensatory mechanisms in hemorrhagic shock can lead to death. Without intervention, a classic trimodal distribution of deaths is seen in severe hemorrhagic shock. An initial peak of mortality occurs within minutes of hemorrhage due to immediate exsanguination. Another peak occurs after 1 to several hours due to progressive decompensation. A third peak occurs days to weeks later due to sepsis and organ failure.

History: History taking should address the following:

• Specific details of the mechanism of trauma or other cause of hemorrhage are essential.

• Inquire about a history of bleeding disorders and surgery.

• Prehospital interventions, especially the administration of fluids, and changes in vital signs should be determined. Emergency medical technicians or paramedics should share this information.

Prehospital Care:

• The standard care consists of rapid assessment and expeditious transport to an appropriate center for evaluation and definitive care.

• Intravenous access and fluid resuscitation are standard. However, this practice has become controversial.

• For many years, aggressive fluid administration has been advocated to normalize hypotension associated with severe hemorrhagic shock. Recent studies of urban patients with penetrating trauma have shown that mortality increases with these interventions; these findings call these practices into question.

• Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage, dislodge partially formed clots, and dilute existing clotting factors. Findings from animal studies of uncontrolled hemorrhage support these postulates. These provocative results raise the possibility that moderate hypotension may be physiologically protective and should be permitted, if present, until hemorrhage is controlled.

• These findings should not yet be clinically extrapolated to other settings or etiologies of hemorrhage. The ramifications of permissive hypotension in humans remain speculative, and safety limits have not been established yet.

Emergency Department Care:

• Management of hemorrhagic shock should be directed toward optimizing perfusion of and oxygen delivery to vital organs.

• Diagnosis and treatment of the underlying hemorrhage must be performed rapidly and concurrently with management of shock.

• Supportive therapy, including oxygen administration, monitoring, and establishment of intravenous access (eg, 2 large-bore catheters in peripheral lines, central venous access), should be initiated.

• Intravascular volume and oxygen-carrying capacity should be optimized.

• In addition to crystalloids, some colloid solutions, hypertonic solutions, and oxygen-carrying solutions (eg, hemoglobin-based and perfluorocarbon emulsions) are used or being investigated for use in hemorrhagic shock.

• Blood products may be required.

• Determination of the site and etiology of hemorrhage is critical to guide further interventions and definitive care.

• Control of hemorrhage may be achieved in the ED, or control may require consultations and special interventions.

Consultations: Consult a general or specialized surgeon, gastroenterologist, obstetrician-gynecologist, radiologist, and others as required.

ACUTE ANEMIA

Anemia is characterized by a reduction in the number of circulating red blood cells (RBCs), the amount of hemoglobin, or the volume of packed red blood cells (hematocrit). Anemia is classified as acute or chronic. Acute anemia denotes a precipitous drop in the RBC population due to hemolysis or acute hemorrhage. In the emergency department (ED), acute hemorrhage is by far the most common etiology. This article also discusses other causes of acute anemia.