The function of the RBC is to deliver oxygen from the lungs to the tissues and carbon dioxide from the tissues to the lungs. This is accomplished by using hemoglobin, a tetramer protein composed of heme and globin. Anemia impairs the ability of the RBCs to transport oxygen and carbon dioxide.
Physiologic response to anemia varies according to acuity and the type of insult. Gradual onset may allow for compensatory mechanisms to take place. With anemia due to acute blood loss, a reduction in oxygen-carrying capacity occurs along with a decrease in intravascular volume, with resultant hypoxia and hypovolemia. Hypovolemia leads to hypotension, which is detected by stretch receptors in the carotid bulb, aortic arch, heart, and lungs. These receptors transmit impulses along afferent fibers of the vagus and glossopharyngeal nerves to the medulla oblongata, cerebral cortex, and pituitary gland.
In the medulla, sympathetic outflow is enhanced while parasympathetic activity is diminished. Increased sympathetic outflow leads to norepinephrine release from sympathetic nerve endings and discharge of epinephrine and norepinephrine from the adrenal medulla. Sympathetic connection to the hypothalamic nuclei increases ADH secretion from the pituitary gland. ADH increases free water reabsorption in the distal collecting tubules. In response to decreased renal perfusion, juxtaglomerular cells in the afferent arterioles release renin in the renal circulation, leading to increased angiotensin I, which is converted by angiotensin-converting enzyme to angiotensin II.
Angiotensin II has a potent pressor effect on arteriolar smooth muscle. Angiotensin II also stimulates the zona glomerulosa of the adrenal cortex to produce aldosterone. Aldosterone increases sodium reabsorption from the proximal tubules of the kidney, thus increasing intravascular volume. The primary effect of the sympathetic nervous system is to maintain perfusion to the tissues by increasing systemic vascular resistance (SVR). The augmented venous tone increases the preload and, hence, the end-diastolic volume, which increases stroke volume. Therefore, stroke volume, heart rate, and SVR all are maximized by the sympathetic nervous system. Oxygen delivery is enhanced by the increased blood flow.
In states of hypovolemic hypoxia, the increased venous tone due to sympathetic discharge is thought to dominate the vasodilator effects of hypoxia. Counterregulatory hormones (eg, glucagon, epinephrine, cortisol) are thought to shift intracellular water to the intravascular space, perhaps because of the resultant hyperglycemia. This contribution to the intravascular volume has not been clearly elucidated.
History
Elicit a thorough and focused history while assessing ABCs and initiating resuscitation. In the critically ill patient, the emergency physician should attempt to obtain a focused history (per the mnemonic AMPLE: allergies; medications, including over-the-counter drugs such as NSAIDs; past medical and surgical history; last meal; and events preceding incident).
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For noncommunicative patients, caretakers, paramedics, or primary physicians are a valuable source of information.
For injured patients, question paramedics about the circumstances of the accident, mechanism of the injury, initial vital signs, estimated blood loss in the field, prehospital treatment initiated, and response.
Patients with chronic illnesses are often knowledgeable about their condition and can provide information about prior complications and treatments. A call to their primary care physician may provide additional information and may help with disposition.
Important specific queries should address GI and menstrual histories (where applicable).
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Specific questions about menstrual timing, frequency, and duration of vaginal bleeding in premenopausal females are required. Denial of the possibility of pregnancy should not preclude a beta-human chorionic gonadotropin (beta-hCG) test in premenopausal females with acute anemia.
When concern for GI hemorrhage exists, obtain a full GI history including stool color, consistency, and frequency. Black, tarry, malodorous, and frequent stools characterize upper GI bleeding proximal to the ligament of Treitz. Maroon, lumpy, irregular stools characterize lower GI bleeding.
Consider constitutional symptoms of chronic illnesses (eg, weight loss, night sweats, rashes, bowel changes).
Consider family history of malignancy or hematologic problems.
Physical
Initial evaluation
Monitor initial vital signs and address any abnormality. Periodic measurement of vital signs and examinations of appropriate organ systems are helpful in assessing ongoing hemorrhage.
In patients with multiple traumas, presume that every body cavity contains blood until investigation suggests otherwise. The chest, abdomen, pelvis, and extremities must undergo thorough physical examination with imaging, as clinically indicated.
Cutaneous findings
In early hemorrhagic shock, capillary refill time may increase and the skin may feel cool to touch. With progressive shock, the skin is cold to touch, and it appears pale and mottled.
Flank ecchymosis (Grey-Turner sign) suggests retroperitoneal hemorrhage, while umbilical ecchymosis (Cullen sign) suggests intraperitoneal or retroperitoneal bleeding. Both are rare findings in acute states.
Patients with jaundice may have liver disease, hemoglobinopathies, or other forms of hemolysis. Purpura and petechiae suggest platelet disorders, and hemarthrosis may be due to hemophilia. Diffuse bleeding from intravenous sites and mucous membranes may be due to disseminated intravascular coagulation (DIC). In patients with alcoholic liver disease, spider angiomata, caput medusae, umbilical hernias, and hemorrhoids may be appreciated.
Neurologic findings
Agitation may present secondary to acute blood loss.
When blood loss exceeds 40% of total volume, the patient may lose consciousness.
Cardiovascular and respiratory findings
With chronic anemia, a hyperdynamic heart, with a prominent point of maximal impulse (PMI), a systolic flow murmur and, occasionally, an S3, may be heard.
Advanced trauma life support classifies shock into 4 levels.
In class I (<15% blood loss), mild tachycardia may be present, but blood pressure is normal.
In class II (15-30% blood loss), tachycardia, tachypnea, and a decreased pulse pressure are seen.
Class III (30-40% blood loss) always leads to a measurable decrease in blood pressure as well as a significant tachycardia and a narrow pulse pressure.
Class IV (40% and greater blood loss) leads to patient demise unless prompt resuscitative measures are taken. Marked tachycardia and significantly decreased blood pressure are common findings.
Blood loss greater than 50% leads to loss of pulse and blood pressure.
Tachypnea may occur with blood loss greater than 15% of total volume (class II).
Patients with exacerbations of chronic anemia occasionally may present with signs and symptoms of congestive heart failure.
Genitourinary findings: Urinary output is decreased in class III shock and is negligible in class IV shock.
Other findings
Organomegaly is a common finding in patients with chronic blood disorders.
A palpable spleen and an enlarged hepatic inferior border (more than 3 cm below the right midclavicular costal margin) may suggest chronic anemia.
Causes
The common pathway in life-threatening acute anemia is a sudden reduction in the oxygen-carrying capacity of the blood. Depending on the etiology, this may occur with or without reduction in the intravascular volume. It is generally accepted that an acute drop in hemoglobin to a level of 7-8 g/dL is symptomatic, while levels of 4-5 g/dL may be tolerated in chronic anemia, as the body is able to gradually replace the loss of intravascular volume.
