Editor de Programas

mon and serious problem in the United States.

A. Classification. Gastrointestinal bleeding is traditionally classified as "upper" or "lower," depending on whether the bleed originates above or below the ligament of Treitz.

B. Definitions

1. Hematemesis is blood, including "coffee grounds," in the vomitus. Hematemesis clearly represents an upper gastrointestinal source.

2. Hematochezia is blood in the stool. Hematochezia can occur with lower gastrointestinal bleeds as well as rapidly bleeding upper gastrointestinal bleeds.

H O T

K E Y

In 1 0% of patients with hematochezia, the source of bleeding is the upper gastrointestinal tract.

3. Melena is black, tarry stool resulting from digested blood. Melena usually indicates an upper gastroin­ testinal bleed because the blood has been digested to hematin, but small bowel and right-sided colonic hemorrhages can also produce melena.

H O T

K E Y

Bismuth subsalicylate, iron, spinach, and charcoal can also produce black stools.

1 70 Chapter 28

III

CAUSES OF GASTROINTESTINAL BLEEDING

A. Upper gastrointestinal source. There are many causes of upper gastrointestinal tract bleeding; the most common can be easily remembered using the mnemonic, "G UM BLEEDING." (The first three causes are the most common.)

Gastrointestinal Bleeding-Upper Gostrointes· tinal Sources ("GUM BLEEDING")

Gastritis (secondary to NSAIDs, olcohol, or stress)

Ulcers (often caused by Helicobacter pylori or NSAIDs)

Mallory-Weiss tear (often secondary to exces­ sive vomiting)

Biliary (hemobilia, usually secondary to trauma)

Large vorices (seen in patients with portal hy­ pertension)

Esophagitis or Esophageal ulcer

Enterooortic fistula (usually seen in patients with aortic grafts)

Duodenitis or Dieulafoy's lesion (an ectatic ar­ tery in the stomach)

Inflammatory bowel disease (upper tract Crohn's disease)

Neovascularization (arteriovenous malforma­ tion), usually seen in the elderly; more com­ monly causes lower gastrointestinal bleeding Gastric cancer

B. Lower gastrointestinal source. Use the following mne­ monic to remember the causes of lower gastrointestinal tract bleeding-you may need a "DRAIN" to collect the blood. V I I I I 1\ :s: � III t:1: 0 0. t:: tl! I=: t:1: (I) :z: V I I

Acute Gostrointestinal Bleeding 1 7 1

Gastrointestinal Bleeding-Lower Gastrointes­ tinal Sources ("DRAIN")

Diverticulosis Radiation colitis

Arteriovenous malformation (angiodysplasia) Ischemia, Inflammation, or Infection Neoplasm

1. Diverticulosis is the most common cause of lower gastrointestinal bleeding. The disorder is painless and is almost never a cause of chronic blood loss.

2. Radiation colitis can occur at any time following radiation therapy.

3. Arteriovenous malformations (angiodysplasia) oc­ cur primarily in the elderly and may cause both acute and chronic blood loss.

4. Ischemic colitis. The patient experiences pain out of proportion to the examination.

S. Inflammatory bowel disease is usually accompanied by diarrhea and rarely causes massive bleeding. 6. Infectious colitis is also usually accompanied by di­

arrhea.

7. Neoplasms (benign or malignant) usually cause

chronic, rather than acute, blood loss.

IIII

APPROACH TO THE PATIENT

A. Patient history. The history is helpful for distinguishing

between an upper and lower source of bleeding, but poor for determining the exact cause of the bleeding. It is important to inquire about the following:

1. Number of episodes

2. Most recent episode

3. Use of nonsteroidal antiinflammatory drugs (NSAIDs)

and aspirin

4. Anticoagulant use S. Cirrhosis

6. Alcohol abuse

7. Vomiting prior to hematemesis

8. Presence and location of abdominal pain 9. Prior aortic surgery

B. Physical examination

1 72 Chapter 28

"tilts" (i.e., moving from a supine posItIon to an upright position causes his pulse to increase by more than 20 beats/min or his systolic blood pressure to decrease by more than 10 mm Hg), then his intravas­ cular volume is 10%-20% helow normal.

H O T

K E Y

Patients on f3 blockers might hove a "normal" pulse rate, despite a large volume loss.

2. HEENT. Check for scleral icterus, which may indi­ cate liver disease with associated varices. Rule out epistaxis and oral lesions as a source of upper gastro­ intestinal tract bleeding.

3. Lungs and heart. Check for evidence of left ven­ tricular dysfunction. which can affect fluid adminis­ tration.

4. Abdomen. Given the cathartic nature of blood, the absence of bowel sounds may suggest an intraabdom­ inal catastrophe. Look carefully for rigidity, involun­ tary guarding, and rebound tenderness, which may suggest peritonitis.

S. Rectum. Palpate for rectal masses. A stool guaiac should be performed if the stools are not clearly bloody.

6. Neurologic examination. Check for asterixis (evi­ dence of liver disease).

7. Skin. Look for signs of liver disease, such as jaundice, spider angiomata, and palmar erythema.

C. Diagnostic tests. Important initial tests to run include:

1. Blood typing and cross-matching

2. Complete blood count ( (,BC) with platelets 3. Electrolyte panel

4. Blood urea nitrogen (BUN) and creatinine levels S. Liver tests

6. Prothrombin time (PT) and partial thromboplastin time {PIT)

7. Chest and abdominal radiographs

8. Electrocardiogram (EKG) V I I I I 1\ V I I

Acute Gastrointestinal Bleeding 1 73

D. General guidelines for the management of a patient with gastrointestinal bleeding. In a patient with gastrointesti­ nal bleeding, do not delay management because you have not figured out the cause of the bleeding! Gastrointesti­ nal bleeding is one situation in internal medicine where the initial management is usually the same regardless of the exact cause.

1. Ensure that the ABCs (airway, breathing, circula­ tion) are in place.

2. Begin fluid replacement. Intravenous access should be obtained immediately, preferably with two large­ bore (18-gauge or larger) intravenous lines.

3. Insert a nasogastric tube if there is any possibility of an upper gastrointestinal bleed. Bolus with 500 cc of water, then withdraw- keep a tab of how much water it takes for the aspirate to become almost clear. a. The nasogastric tube aspirate may be negative,

even in the presence of upper gastrointestinal bleeding, if:

(1) The source of the bleeding is below the end of the nasogastric tube (e.g., if the nasogastric tube ends in the stomach, bleeding from a duodenal ulcer may not be apparent in the as­ pirate).

(2) The bleeding is transient.

b. The tube should be kept in place if there is active bleeding or signs of a small bowel obstruction.

4. Hold antihypertensive or diuretic therapy. In addi­ tion, the patient should receive nothing by mouth. S. Decide whether or not to admit the patient to the

intensive care unit (ICU).

a. If your patient needs to take a trip to the ICU, she will need a "VISA." Patients generally require admission if any of the following criteria are met:

Criteria for Admittance to ICU with a Gastroin· testinal Bleed ("VISA")

Variceal bleeding (suspected or confirmed) Instabilily of vital signs

Serious comorbid conditions (e.g., coronary artery disease, COP D)

1 74 Chapter 28

b. All patients admitted to the ICU should be seen hy a gastroenterologist immediately.

6. Stabilize the patient.

a. Transfusion

(1) Elderly patients or thuse with coronary ar­ tery disease are usually transfused to keep their hematocrit greater than 30%. At least two units of typed and cross-matched packed red blood cells (RBCs) should be kept in the blood bank at all times.

(2) In a patient with active bleedi�g, consider a platelet transfusion if the patient's platelet count is less than 50.000/mm>. Fresh frozen plasma should be used if the patie�t's inter­ national normalized ratio (INR) IS greater than 1 .5.

H O T

K E Y

A unit of blood entering or leaving the body should change the patient's hemoglobin by approximately

1 g/di.

b. Intravenous H2 blockers are usually adminis­ tered.

c. Vitamin K should be administered if the patient's PT or PTT is abnormal.

7. Perform ancillary tests if necessary.

a. A technetium-99 (ro)-Iabeled red blood cell scan can be performed if a slow (i.e., 0. 1 -1 ml! min) lower gastrointestinal bleed is present. . b. An angiogram may be indicate

�

wh�n a rapid

(i.e., > I mllmin) lower gastromtestmal bleed is suspected. V I I I I 1\ :s: � III 1:1: 0 0. t:: tl! J::: 1:1: (l) :z: v I I

29. _Splenomegaly

• ••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••• O'

a

III

INTRODUCTION

A. Splenomegaly is enlargement of the spleen.

1. A normal spleen is 12 em by 7 em and weighs less than 200 grams. It is surrounded by a thin capSUle. The spleen is usually not palpable unless it is en­ larged; therefore. a palpable spleen is always ab­ normal.

2. Massive splenomegaly occurs when the spleen weighs more than 3000 grams.

B. Hypersplenism is the term given to any clinical situation in which the spleen inappropriately removes excess amounts of leukocytes, platelets. or erythrocytes from the circulation.

1. Hypersplenism and splenomegaly are not synony­

mous. Patients with hypersplenism all have spleno­

megaly; however, only a small percentage of those with splenomegaly have hypersplenism.

2. Characteristics of hypersplenism include the fol­ lowing:

a. Splenomegaly

b. Splenic destruction of one or more cell lines

c. Normal or hyperplastic bone marrow

d. Reversal of the cytopenia following splenectomy

CLINICAL MANIFESTATIONS OF SPLENOMEGALY A. Nonacute splenomegaly is most common. Clinical pre­

sentations include:

1. Early satiety (because of impaired gastric filling);

may lead to weight loss

2. Cytopenia (as a result of hypersplenism); may

lead to infections, bleeding. or fatigue

3. Symptoms of the underlying disease

B. Acute splenomegaly

1. Clinical signs include the sudden onset of left upper quadrant pain and a tender. enlarged spleen.

2. Differential diagnoses

a. Subcapsular hematoma

b. Splenic rupture due to trauma (even remote) or an infectious process (e.g., malaria, mononucleo­ sis, typhoid fever)

1 76 Chapter 29

c. Splenic infarct due to sickle cell disease or em­ bolism

d. Hemorrhage into a splenic cyst

IIII

CAUSES OF SPLENOMEGALY

A. Congestive causes. This category includes any disease that leads to disordered splenic blood flow, so that the blood "backs up" in the spleen. Think of causes that anatomically head away from the spleen.

1. Splenic vein obstruction

2. Portal vein obstruction 3. Hepatic schistosomiasis 4. Cirrhosis

5. Hepatic vein obstruction

6. Constrictive pericarditis

7. Congestive heart failure (CHF) _.

B. Reactive causes. This category includes those diseases

that lead to splenic hyperplasia. Because the spleen is a lymphoid gland, many diseases that cause a systemi.c immunologic response can cause splenomegaly. In addi­ tion, blood disorders that lead to hemolysis can also cause the spleen to enlarge.

1. Infections

a. Bacterial (e.g., endocarditis, tuberculosis, sus­ tained bacteremia)

b. Viral (e.g., mononucleosis, viral hepatitis)

c. Parasitic (e.g., malaria, leishmaniasis, trypanoso­ miasis)

d. Fungal (e.g., disseminated histoplasmosis)

2. Collagen vascular diseases _.

a. Rheumatoid arthritis. Felty's syndrome IS the triad of granulocytopenia, rheumatoid arthritis, and splenomegaly.

H O T

K E Y

Rheumatoid arthritis-like congestive heart failure, sys· temic lupus erythematosus, endocarditis-usually causes mild splenomegaly.

I I 1\ V I I I I 1\ V I I Splenomegaly 1 77

b. Systemic lupus erythematosus (SLE)

3. Serum sickness. This immune complex disorder­ usually caused by a drug hypersensitivity reaction­ occurs 1 -3 weeks following primary exposure (or within 36 hours of re-exposure) to an offending agent.

Clinical Manifestations of Serum Sickness ("SALT")

Skin rosh (morbilliform, urticarial, or palpo­ ble purpura)

Arthralgias or Arthritis

Lymphadenopathy Temperature increase

4. Work hypertrophy can be caused by hemolysis. C. Infiltrative causes 1. Benign H O T K E Y a. Sarcoidosis b. Amyloidosis

c. Gaucher's disease, an autosomal recessive disor­ der characterized by an accumulation of sphin­ golipid within phagocytic cells throughout the body

Hip fracture + Polpable spleen + Eastern European

descent = Goucher's disease

2. Malignant a. Lymphomas

b. Leukemias

c. Myeloproliferative disorders d. Primary splenic tumors e. Metastatic tumors

1 78 Chapter 29

Causes of Massive Splenomegaly ("Hopefully, My Medical Students Can learn Gastroenter­ ology")

Hairy cell leukemia (uncommon, resembles chronic lymphocytic leukemia)

Malaria

Myeloid metaplasia with myelofibrosis (one of four myeloproliferative disorders)

Sarcoidosis

Chronic myelogenous leukemio (onother mye­ loproliFerative disorder)

Lymphomo (primarily splenic lymphoma) Gaucher's disease

ApPROACH TO THE PATIENT

A. Patient history. When taking the history, you .should focus on searching for an underIymg cause. Thmgs to look for include:

1. Alcohol use or cirrhosis

2. CHF

3. Febrile illness (current or recent)

4. Arthralgias, arthritis, or joint stiffness

5. Fever, weight loss, diaphoresis, or lymph node swelling

6. Family history of anemia or splenomegaly

B. Physical examination. Look for evidence of hepatomeg­ aly, lymphadenopathy. skin rash, subcutaneous nodules, CHF, liver disease, or an infectious process.

C. Laboratory tests usually include a complete blood count (CBC) and analysis of the peripheral smear and liver tests.

D. Other tests. Blood cultures may be warranted. An ultra­ sound is useful to confirm the presence of splenomegaly and evaluate the liver size. Bone marrow biopsy, lymph node biopsy, serologies, exploratory laparotomy, and

other imaging studies may also be performed.

V I I I I 1\ V I I

30. Ascites

•••••••••••••• ••••••••••••••••• ,u ••••• ••••••••••••••••••••••• •••••••••••••••••••••••••••••••••••••••••••••••• 'O.

a

III

INTRODUCTION. Ascites is the accumulation of excess fluid within the peritoneal cavity.

CAUSES OF ASCITES. _{Ascites may occur as part of ana­}

sarca (generalized edema) or as an isolated fluid collection.

A. Anasarca. The causes of a generalized edematous state can be remembered as the "osis group"-nephrosis, cir­ rhosis, cardiosis, and hypothyroidosis.

8. Isolated fluid collection. There are three primary mecha­ nisms of ascites production. In addition. there are miscel­ laneous disorders that cause ascites by various mecha­ nisms.

1. Increased hydrostatic pressure in the splanchnic cap­ illaries may result from diseases that produce ele­ vated venous pressure. One way of thinking about the causes of increased hydrostatic pressure is to trace the venous blood from the heart down. a. Cardiac. Right-sided heart failure and constric­

tive pericarditis lead to elevated venous pressure and can cause ascites.

b. Hepatic

(1) Postsinusoidal obstruction includes inferior vena cava obstruction, hepatic vein obstruc­ tion (i.e., Budd-Chiari syndrome), or hepatic venule obstruction (i.e .. veno-lIcclusive dis­ ease).

(2) Sinusoidal obstruction is the most common cause of ascites and usually results from cir­ rhosi<i.

(3) Presinusoidal obstruction may be caused by schistosomiasis or portal vein thrombosis. (Portal vein thrombosis may cause variceal bleeding, but only rarely produces ascites.) 2. Oecreased oncoti(' pressure may result from de­ creased albumin intake (i.e .. starvation), decreased albumin production (i.e., severe liver disease). or increased loss of alhumin (e.g., nephrotic syndrome, protein-losing enteropathy).

3. Increased capillary permeability may occur with in­ fection (e.g., tuberculosis) or malignancy.

1 80

IIII

Chapter 30

4. Miscellaneous causes

a. Hypothyroidism. Myxedema usually produces anasarca, not isolated ascites.

b. Pancreatitis may cause pancreatic ascites.

c. Lymphatic obstruction from trauma, tumor. or

infection (e.g., filariasis, tuberculosis) may cause

chylous ascites.

ApPROACH TO THE PATIENT

A. Patient history and physical examination. A complete history and physical examination (including rec

�

al and pelvic examinations) are necessary. B y rem�mbenng the underlying mechanisms, you can systematically pursue the diagnosis.

1. Increased hydrostatic pressure

a. Right-sided heart failure or constrictive pericar­ ditis. Ask about symptoms of left-sided heart fail­ ure (the most common cause of right-sided heart failure). Perform a careful cardiac examination and evaluate the jugular venous pressure.

b. Budd-Chiari syndrome may be suggested by right upper quadrant pain and an enlarged liver in a patient with a myeloproliferative disorder. . c. Hepatic veno-occJusive disease should be consid­

ered in patients with ascites and a history of che­ motherapy Or bone marrow transplantation.

d. Cirrhosis is the most common cause of ascites.

Inquire about risk factors, including alcohol con­ sumption and hepatitis exposures (e.g., i?tr�ve­ nous drug use). Look for signs of chromc liver

disease (see Chapter 32). _.

2. Low oncotic pressure in the absence of severe liver disease may be suggested by a history of starvation or by the presence of nephrotic syndrome.

3. Increased capiJJary permeability may be suggested by a history of fevers or weight loss, which could suggest infection or malignancy.

4. Miscellaneous mechanisms

a. Pancreatic ascites should be considered when­ ever pancreatitis is a possibility.

b. Lymphatic obstruction is suspected on the basis of the "milky" appearance of chylous ascites.

c. Myxedema. If myxedema is the etiology, the pa­ tient will usually have other symptoms of hypo­ thyroidism (see Chapter 74).

V I I I I 1\ V I I Ascites 1 8 1

B. Laboratory tests. Routinely performed laboratory tests

include a complete blood count (CBC) with differential, an electrolyte pane!, blood urea nitrogen (BUN) and creatinine levels, prothrombin time (PT) and partial thromboplastin time (PTT), and liver function tests with serum albumin. A urine dipstick test for protein and thyroid function tests are also frequently performed, es­ pecially when anasarca is present.

C. Diagnostic paracentesis is almost always needed to make

a diagnosis. Even when the diagnosis seems apparent, diagnostic paracentesis is still indicated to rule out sec­ ondary processes [e.g., spontaneous bacterial peritoni­ tis (SBP)].

I. Procedure

a. Make sure that the patient has emptied his blad­ der before the procedure. Alternatively, a Foley catheter may be inserted.

b. A midline approach (i.e., 1-2 cm directly below the umbilicus) may be preferable because this region is avascular. However, prior midline sur­ gery often necessitates a lateral approach be­ cause the bowel may be adherent to the perito­ neal wall.

c. A small needle (19-gauge or smaller) is usually used.

2. Evaluation. A cell count with differential, bacterial

Gram stain and cultures, and an albumin level should be obtained on the fluid sample. Lactate dehydroge­ nase (LDH) and glucose levels may provide addi­ tional information. An amylase or triglyceride level should he ordered if there is a possibility of pancre­ atic or chylous ascites, respectively.

H O T

K E Y

Remember to order a serum albumin level at approxi­ mately the same time the ascitic flUid is obtained.

3. Interpretation. Table 30-1 contains likely etiologies of ascitcs and their characteristic fluid findings.

Cirrhosis 2: l.1 < 250 (mesothelial) Moderate Abnormal liver function tests

Spontaneous bacterial 2: l.1 > 250 (PMNs) Moderate Culture may be positive peritonitis (SBP)

Congestive heart failure ;;, 1.1 < 1000 (mesothelial) High Elevated neck veins, gallops, abnormal EKG

Hypothyroidism 2:11 < _{250 (variable)} Variable Decreased free T., increased TSH

liver malignancy (pri- ;;, l.1 _{Variable Moderate Elevated serum AFP with primary malignancy}

mary or secondary)

Nephrotic synd rome <1.1 < 250 (mesothelial) low Positive urine dipstick and 24-hour collectian far

protein

Tuberculous ascites < l.1 > _{1000 (variable)} High Ascitic acid-fast bacillus stain occasionally positive

Secondary peritonitis <1.1 > 250 (PMNs) Moderate Very low ascitic glucose, palymycrobial Pancreatic ascites < 1.1 > 1000 (PMNs) Maderate Increased serum and fluid amylase

Peritoneal malignancy < 1.1 > 1000 (variable) High Cytology, CT scan, peritoneal biopsy may be

useful

AFP = a-fetoprotein; EKG = electrocardiogram; PMNs = polymorphonuclear neutrophils; T. = thyroxine; TSH = thyraid-stimulating

hormone.

* Total protein is considered low if it is less than 1 g/ dl, moderate if it is 1-3 g/ dl, and high if it is >3 g/ dl.

co N () :r o "0 � W o

Ascites

HOT

KEY

183 Remember that the findings given are only general­ izations and will not apply in all cases. Furthermore. the presence of two or more disorders may skew the fluid analysis.

a. Cell count. The cell count can be used to evaluate the possibility of SBP, tuberculosis, or malig­ nancy.

(1) SBP. Empiric treatment for SBP is usually indicated when the absolute neutrophil count exceeds 250 celiS/ill. Counts greater than 500 cells/p,l are more specific but less sensitive for SBP.

(2) Tuberculosis or malignancy. A cell count that exceeds 250 cells/ILl and is lymphocyte pre­ dominant often implies tuberculous or malig­ nant ascites.

b. Serum-ascites albumin gradient. Subtract the as­ citic fluid albumin value from the serum albu­ min value.

(1) If the result is greater than or equal to 1.1, portal hypertension is implicated (i.e., a hy­ drostatic etiology is responsible).

(2) If the value is less than 1.1, capillary perme­ ability is probably abnormal (i.e., infection or malignancy may be implicated).

If portol hypertension is occompanied by onother disor­ der that produces increased copillary permeobility, the gradient will usually remain greoter than or equal to 1 .1 . SBP usually occurs in potients with portal hyperten­ sion; therefore, the gradient is usually greater than or equal to 1.1 in these patients.

c. Gram stain and culture of ascitic fluid should be performed if peritonitis is suspected.

d. LDH and glucose levels. An elevated LDH or low glucose level may indicate tuberculosis or malignancy.

e. Amylase and triglyceride levels. Elevated amy­ lase or triglyceride levels may indicate pancreatic or chylous ascites, respectively.

184 Chapter 30

D. Additional testing may be necessary when the ascitic fluid contains an elevated cell count with a lymphocyte predominance, increasing suspicion for tuberculous or malignant ascites.

1. Purified protein derivative (PPD) test. A positive PPD test will increase suspicion for tuberculous peri­ tonitis.

2. Acid-fast bacillus stain and culture of ascitic Huid. These are relatively insensitive tests, but sending a large volume of fluid (e.g., ] L) may increase the yield.

3. Ascitic Huid cytology is also of relatively low yield unless a large volume of fluid is sent.

4. Abdominal computed tomography may reveal an in­ tra-abdominal malignancy.

5. Laparoscopy with peritoneal biopsy is often per­ formed to make an expedient diagnosis.

TREATMENT. _{The general management of ascites is dis­} cussed in Chapter 33 IV B 4; other specific therapies are tailored to the underlying etiology and will not be dis­ cussed here. I I /\ V I I I I /\ V I I

31.Acute Pancreatitis

a

INTRODUCTION. _{Pancreatitis implies inHammation of the} pancreas.

A. Acute pancreatitis results from the leakage of pancreatic enzymes into pancreatic tissue, leading to autodigestion.

In document 3.1 Características Externas 3.2 Características Internas 3.3 Mantenimiento Preventivo (página 36-43)