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The percentage of the BSA that is burned is estimated by the “rule of nines” (Fig. 21 -2).

Half of the calculated amount of fluid is given in the first 8 hours, and the remaining half is distributed over the succeeding 16 hours.

The volume and rate of fluid administration should be varied, if necessary, depending on the central venous pressure, urine output, and other vital signs.

Optimal urine output is 30–50 mL/hour in adults and 1 mL/kg of body weight/hour in children.

To aid urine flow and to allow monitoring of output, an indwelling urethral catheter should be inserted early, even in children.

Evaporative hypotonic fluid loss is evident after the first 24 hours.

Intravenous fluids at a rate to maintain serum sodium concentration at 140 mEq/L (approximately 4–5 L in a 70 -kg patient with 50% burn)

Colloid (controversial) at a rate of 0.3–0.5 mL plasma/kg body weight/% burn

D Burn wound care

Cold compresses may be applied to relieve the pain of partial-thickness burns if the burns cover less than 10% of the BSA. If burns cover a large area, cold compresses or immersion in water will cause an unacceptable lowering of the body temperature with associated problems.

Maintenance of body temperature is important, especially in children, who have a high evaporative heat loss and may rapidly become hypothermic.

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Shielding the burn from air movement by covering it with a clean, warm linen dressing will help to relieve the pain of partial-thickness burns.

Topical antimicrobial treatment with agents such as silver nitrate solution is usually recommended for deep second-degree and third -degree burns. However, only specific antibacterial burn wound medications should be applied to the burn.

Debridement and escharectomy are best performed in specialized centers; however, escharotomy may be urgently required in circumferential extremity wounds, causing distal circulatory impairment, and in circumferential trunk or neck wounds, causing respiratory impairment.

E Other considerations

Other considerations in the care of burn patients

NG intubation is indicated for any patient with nausea or vomiting and for most patients with burns covering 25% or more of the BSA.

Analgesia should be confined to conservative use of intravenous narcotics in small, frequent doses.

Systemic antibiotics are usually not indicated. However, in some situations, particularly in the early treatment of patients with partial-thickness burns, prophylaxis against β-hemolytic streptococci is warranted.

Tetanus toxoid with or without hyperimmune human globulin should be given if the patient's immunization

status is not current (according to ACS guidelines).

Chemical burns

Alkali burns are generally deeper and more serious than acid burns.

All chemical burns should be treated by flushing with neutral solutions.

Immediate drenching in a shower or with a hose is helpful.

Burns of the eye require extensive flushing over an 8-hour period.

Electrical burns are usually deeper and more severe than indicated by the surface appearance.

Muscle and soft tissue injury. Electrical energy is converted to heat as it traverses the body along the path of least resistance (i.e., blood vessels and nerves). Thus, muscles closest to bone––which has a high resistance and, therefore, generates the most heat––incur the most damage.

Muscle involvement may be markedly underestimated by attention to the surface wounds alone (e.g., fluid requirements are about 50% higher than estimated by surface wounds).

Brawny edema is characteristic.

Early escharotomy, fasciotomy, and debridement are often necessary, and repeated explorations at 24–48 hours may be needed.

Serious soft tissue injury results from high -voltage electrical burns (generally considered more than 1,000 volts); low-voltage electrical burns (household outlets) cause less soft tissue injury but may cause asystole and apnea.

Surface burns occur at both the entrance and exit points of the current. Unsuspected exit sites, including the scalp, feet, or perineum, should be sought.

Oliguria is common, as is acidosis.

Urine output should be maintained at high levels—at least 100 mL/hour in adults. Mannitol administration is usually needed to maintain this level and is mandatory in the presence of myoglobinuria.

Arterial blood pH should be monitored and maintained with intravenous bicarbonate, given as 50 mEq every half hour until the pH reaches normal levels.

Myocardial infarction (immediate or delayed) is well-described postinjury, thus making continuous cardiac monitoring essential in all patients with electrical burns.

Transverse myelitis and cataracts are long-term sequelae.

Chapter 22

Spleen

R. Anthony Carabasi III

John C. Kairys

John S. Radomski

I Introduction

A Anatomy

Developmental considerations

The spleen develops from mesenchymal tissue in the dorsal mesogastrium. This tissue rotates to the left as development progresses. By the end of the third gestational month, the organ is formed. The point at which the spleen remains attached to the dorsal mesogastrium becomes the gastrosplenic ligament.

The organ itself consists of an outer capsule and trabeculae, which enclose the pulp. The pulp consists of three zones:

The white pulp is essentially a lymph node. It contains lymphocytes, macrophages, and plasma cells in a reticular network.

The red pulp consists of cords of reticular cells with sinuses in between.

The marginal zone is a poorly defined vascular space between the pulps.

The adult spleen weighs between 100 g and 150 g and measures 12 × 7 × 4 cm.

Location. The spleen is located in the left upper quadrant of the abdomen and is protected by the eighth to the eleventh ribs. It is bordered by the left kidney posteriorly, the diaphragm superiorly, and the fundus of the stomach and the splenic flexure of the colon anteriorly.

Vasculature

The main blood supply is the splenic artery , which is a branch of the celiac axis. It travels along the superior border of the pancreas. At the hilus, it branches into trabecular arteries, which terminate in small vessels to the splenic pulp.

The splenic vein crosses behind or at the lower border of the pancreas. It joins the superior mesenteric vein to form the portal vein (Fig. 22 -1).

B Physiology

The spleen has multiple functions, some of which remain poorly understood. Its most important functions are its ability to act as a blood filter and its role in the immunologic process of the body.

Filtering functions. Splenic blood flow is approximately 350 L/day of blood. Most blood elements pass through rapidly and uneventfully.

Removal of old or abnormal red blood cells

The spleen removes about 20 mL/day of aged or abnormal red blood cells.

Secondary hypersplenism is caused by an identifiable underlying disease, such as:

Disorders of splenic blood flow

Hematopoietic disorders leading to increased red blood cell turnover

Immune disorders

Infiltrative disorders

Infectious diseases

Neoplastic diseases

C Presentation

Anemia, leukopenia, or thrombocytopenia may be noted on a routine laboratory workup.

Anemia may lead to pallor, fatigue, and dyspnea.

Leukopenia may lead to increased susceptibility to infection.

Thrombocytopenia is characterized by easy bruising and epistaxis.

Splenomegaly may be found incidentally during the physical examination or in a radiologic imaging study.

The patient may present with pain secondary to splenic enlargement or rupture.

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D Evaluation

Peripheral blood smears may demonstrate a decreased number of red blood cells, white blood cells, or platelets.

Reticulocytosis is frequently observed if the hypersplenism is causing an increased turnover of red blood cells.

Abnormal red blood cell morphology is sometimes diagnostic for the underlying hematologic disorder (e.g., spherocytosis).

Bone marrow aspirate

A compensatory increase in megakaryocytes should be observed if there is sequestration of platelets in the spleen.

Abnormalities of hematopoiesis may be identified as well.

Radiologic imaging

An ultrasound or a computed tomography (CT) scan can accurately document the size of the spleen as well as determine any structural abnormalities. Other findings on the scans may suggest an underlying disease process.

Radioisotope scans may demonstrate a shortened half -life for circulating blood elements and their sequestration in the spleen.

Immunologic tests using specific antibodies may be diagnostic for certain diseases, particularly those with an autoimmune basis.

E

Treatment depends on the underlying condition. Table 22 -1 summarizes the role of surgery in various pathologic conditions.

TABLE 22-1 Absolute and Relative Indications for Splenectomy

Spontaneous rupture

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III Pathologic Conditions Affecting the Spleen

A Primary splenic disorders

Primary hypersplenism is essentially a diagnosis of exclusion; it is made only after possible causes of secondary hypersplenism have been ruled out.

It is rare, and it affects mainly women.

There is an exaggerated destruction or sequestration of circulating blood elements.

Any one or all of the formed blood elements may be involved.

The hematologic findings may be accompanied by recurrent fevers and infections.

Splenomegaly is almost always present.

It may, in some cases, actually be an early manifestation of lymphoma or leukemia.

The treatment is splenectomy. Steroids do not improve the condition.

Splenic cysts may be idiopathic or, more commonly, may result from previous trauma. Surgery is indicated if the cysts become large enough to cause pain or torsion or if they exert a significant mass effect on surrounding structures. With simple cysts, unroofing is sufficient, thus preserving splenic function.

B Disorders of splenic blood flow

Portal hypertension may cause passive splenic congestion.

It is the most common mechanism of secondary hypersplenism.

Causes of portal hypertension include alcoholic cirrhosis, viral hepatitis, Budd -Chiari syndrome, and congestive heart failure.

Hypersplenism associated with portal hypertension is usually mild and clinically insignificant. Only 15% of patients develop significant hypersplenism; therefore, isolated splenectomy is generally not indicated.

Splenic vein thrombosis can cause secondary hypersplenism with massive splenomegaly.

Cause. Pancreatitis is the usual cause of the thrombosis.

Presentation. The patient may present with bleeding from esophageal or, more characteristically, proximal gastric varices.

Treatment. The hypersplenism and bleeding varices are cured by splenectomy.

Splenic artery aneurysm (see Chapter 7)

C Hematopoietic disorders

Hereditary spherocytosis is one of a group of hereditary hemolytic anemias that cause the most severe symptoms.

Characteristics

Hereditary spherocytosis is characterized by a defect of the red blood cell membrane that results in loss of red blood cell surface area, which causes the cell to be spherical (hence the name), small, and more susceptible to lysis than normal red blood cells.

The cell membrane is thick and rigid, which causes the cells to be held in the splenic pulp. This holding of cells leads to cell lysis, due to deprivation of glucose and adenosine triphosphate (ATP), and occurs only in the spleen.

It is transmitted as an autosomal dominant trait.

Symptoms

Symptoms of hereditary spherocytosis include malaise, abdominal discomfort, jaundice, anemia, and splenomegaly.

The disease may be complicated by gallstones (which are rare in patients younger than 10 years of age) and by chronic leg ulcers that heal only after splenectomy.

Diagnosis is based on the preceding clinical findings and the results of laboratory studies, which include a demonstration of the following:

Spherocytes and an elevated reticulocyte count on a Wright-stained blood smear

Increased osmotic fragility of the red blood cells

Chromium 51 (51 Cr)-tagged red blood cells, which have a greatly shortened half -life and are sequestered in the spleen

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Treatment is splenectomy.

This procedure cures the anemia and jaundice in all patients. Failure of splenectomy to cure the patient is normally caused by an accessory spleen that has been overlooked during the operation.

The operation should be delayed until 4 years of age, if possible, to decrease the chance of postsplenectomy sepsis (see V F 1).

The gallbladder should be removed at the time of splenectomy if gallstones are present.

Other congenital hemolytic anemias. Although splenectomy is not curative, it is indicated occasionally because it reduces the need for multiple transfusions in the following conditions:

Enzyme deficiencies, such as glucose -6-phosphate dehydrogenase (G6PD) deficiency and pyruvate kinase deficiency