IRRITABLE BOWEL SYNDROME

A functional disorder of the motility of the intestines No organic disease or anatomic abnormality More common in women than in men Related factors: o Heredity o Psychological stress o Illness o Diet high in irritating foods o Alcohol consumption o Smoking PATHOPHYSIOLOGY Results from a functional disorder of intestinal motility. This may be related to: o Neurologic regulatory system o Infection or irritation o Vascular or metabolic disturbance Peristaltic waves are affected at different segments of the intestine and in the intensity with which they propel the fecal matter forward Assessment: Primary symptom is alteration in bowel patterns constipation, diarrhea, or a combination of both Often accompanied by pain, bloating, abdominal distention, Abdominal pain is often precipitated by eating and is often relieved by defecation Diagnostic Exams: o Barium Enema o Manometry and electromyography o Stool studies, contrast x-ray studies, protoscopy Medical Mangement Goals of treatment: Relieve abdominal pain Control diarrhea and/or constipation Reduce stress Avoid irritants (beans, caffeinated products, fried foods, alcohol, spicy foods) A well-balanced, high fiber diet is prescribed to hlp control diarrhea and constipation Exercise can assist in reducing anxiety and increasing intestinal motility Hydrophilic colloids (bulk) and antidiarrheal agents may be given to control the diarrhea and fecal urgency. Antidepressants can assist in treating underlying anxiety and depression Anticholinergics and calcium channel blockers decrease smooth muscle spasm, decreasing cramping and constipation Nursing Management: Provide patient and family education o Emphasis is placed on teaching and reinforcing food dietary habits o Patient is encouraged to eat at regular times and chew food thoroughly o Patient should understand although adequate fluid is intake is necessary, fluid should not be taken with meals to avoid abdominal distention. o Alcohol use and cigarette smoking is discouraged

HEPATIC FAILURE
is a condition in which the rapid deterioration of liver function results in coagulopathy and alteration in the mental status of a previously healthy individual. According to time-length between first signs of liver disease and development of encephalopathy: Fulminant: acute liver disease with encephalopathy within 8 weeks of first sign of liver disease. Acute: up to 28 days Subacute:5-12 weeks Drug-related hepatotoxicity is the leading cause of acute liver failure Pathophysiology
acetaminophen overdose idiosyncratic drug reaction viral hepatitis ingestion of amanita falloides maushroom ammonia levels impaired osmoregulation in the brain cerebral edema ICH cerebral blood flow vasodilation Wilsons disesase Reye syndrome HELLP syndrome malignancies nitric oxide levels

neurologic damage brain death DEATH

circulatory insufiiciency & poor organ perfusion multisystem organ failure

Assessment: Jaundice is often but not always present. Right upper quadrant tenderness is variably present. An enlarged liver may be seen with congestive heart failure, viral hepatitis, or Budd-Chiari syndrome. Development of cerebral edema ultimately may give rise to manifestations of Complete blood cell (CBC) count: Results may indicate thrombocytopenia PT and/or international normalized ratio (INR) o These tests are used to determine the presence or severity of coagulopathy. Hepatic enzymes o Levels of the transaminases (aspartate aminotransferase [AST]/serum glutamic-oxaloacetic transaminase [SGOT] and alanine aminotransferase [ALT]/serum glutamic-pyruvic transaminase [SGPT]) are often elevated dramatically as a result of severe hepatocellular necrosis. Serum bilirubin o Elevated in fulminant hepatic failure o It climbs as hepatic dysfunction worsens. Serum ammonia o This level may be elevated dramatically in patients with fulminant hepatic failure. o Arterial blood is the best way to measure ammonia. Serum glucose: levels may be very low and pose a serious hazard. This results from impairments in glycogen production. Serum lactate o Levels are often elevated as a result of both impaired tissue perfusion (increases production) and decreased clearance by the liver. Serum creatinine: levels Blood cultures Serum-free copper o Serum-free copper studies are important to consider when Wilson disease must be excluded or confirmed. Fulminant hepatic failure from Wilson disease appears

increased intracranial pressure (ICP), including papilledema, hypertension, and bradycardia. ascites, Hematemesis or melena Hypotension Tachycardia Laboratory Studies to be uniformly fatal without transplantation. Serum phosphate Viral serologies Acetaminophen level Imaging Studies Liver ultrasonography (Doppler) o Liver ultrasonography establishes the presence of ascites. Computed tomography (CT) scanning or magnetic resonance imaging (MRI) of the abdomen o Intravenous contrast may compromise renal function. Consider performing a contrastfree study. CT scanning of the head helps identify cerebral edema and exclude intracranial mass lesions (especially hematomas) that may mimic edema from fulminant hepatic failure. Also consider and exclude subdural hematomas Procedures Liver biopsy: o A percutaneous liver biopsy is contraindicated in the setting of coagulopathy. However, a transjugular biopsy is helpful for diagnosis if autoimmune hepatitis, metastatic liver disease, lymphoma, or herpes simplex hepatitis is suspected. Intracranial pressure monitoring o When establishing a diagnosis of ICH or cerebral edema, this approach is frequently necessary and has value in guiding management. o Typically, extradural catheters are safer than intradural catheters. Intradural catheters are somewhat more accurate and, in the hands of a neurosurgeon experienced with their use, may be equally safe. Complications Hepatic encephalopathy

Manage hepatic encephalopathy in the conventional way, by providing lactulose and avoiding sedatives. In the late stages of encephalopathy, avoid providing lactulose by mouth or nasogastric tube without previous intubation, considering the risk of aspiration. Cerebral edema Patients in the advanced stages of encephalopathy require close follow-up care. Monitoring and management of hemodynamic and renal parameters, as well as glucose, electrolytes, and acid/base status, become critical. Frequent neurologic evaluation for signs of elevated ICP should be conducted. ICP monitoring ICP monitoring helps in the early recognition of cerebral edema. The ultimate goal of such measures is to maintain neurologic integrity and to prolong survival while awaiting receipt of a donor organ or recovery of sufficient functioning hepatocyte mass. Correct coagulopathy and bleeding tendencies with the use of FFP and platelet infusion. ICH Administration of IV mannitol (in a bolus dose of 0.5-1 g/kg or 50-100 g) is recommended to treat ICH in acute liver failure. Seizures, which may be seen as a manifestation of the process that leads to hepatic coma and ICH, should be controlled with phenytoin Hemorrhage o This develops as a result of the profoundly impaired coagulation that manifests in these patients. o Gastrointestinal bleeding may develop from esophageal, gastric, or ectopic varices as a result of portal hypertension. Portal hypertensive gastropathy and stress gastritis may also develop. Management The most important step is to identify the cause of liver failure. It is also critical to identify those patients who will be candidates for liver transplantation. Another important aspect of treatment in patients with acute liver failure is to provide good intensive care support. Patients with grade II encephalopathy

should be transferred to the intensive care unit (ICU) for monitoring. Maintenance of nutrition and prompt recognition of gastrointestinal bleeding are crucial. Coagulation parameters, CBC count, and metabolic panel should be checked frequently. Serum aminotransferases and bilirubin are generally measured daily to follow the course of infection. Intensive care management includes recognition and management of complications. Maintenance of patent airway o As the patients with fulminant hepatic failure drift deeper into coma, their ability to protect their airway from aspiration decreases. o Patients who are in stage III coma should have a nasogastric tube (NGT) for stomach decompression. o When patients progress to stage III coma, intubation should be performed. Encephalopathy and cerebral edema o Patients should be positioned with the head elevated at 30. o Efforts should be made to avoid patient stimulation. Maneuvers that cause straining or, in particular, Valsalva-like movements may increase ICP. o Reducing elevated ammonia levels with enteral administration of lactulose help prevent or treat cerebral edema. o ICP monitoring helps in the early recognition of cerebral edema. o The ultimate goal of such measures is to maintain neurologic integrity and prolong survival while awaiting receipt of a donor organ or recovery of sufficient functioning hepatocyte mass. Cardiovascular monitoring o A SwanGanz catheter should be placed and fluid replacement with colloid albumin should be guided by the filling pressure. If needed, dopamine or norepinephrine can be used to correct hypotension. Management of coagulopathy o In the absence of bleeding, it is not necessary to correct clotting abnormalities with fresh frozen plasma (FFP); the exception is when an invasive procedure is planned or in the presence of profound coagulopathy.

Recombinant factor VIIa may be used in patients whose condition is nonresponsive to FFP Managing poisonings (eg, acetaminophen, mushroom) requires specific treatment distinct from other, more general issues related to fulminant hepatic failure. o Treat acetaminophen (paracetamol, APAP) overdose with N-acetylcysteine (NAC). o A phalloides mushroom intoxication is much more common in Europe as well as in California. Treat with IV penicillin G, even though its mode of action is unclear. Silibinin, a water-soluble derivative of silymarin, may be administered orally, and oral charcoal may be helpful by binding the mushroom toxin. o Patients with acute liver failure are, by necessity, nothing by mouth (NPO). They may require large amounts of IV glucose to avoid hypoglycemia. When enteral feeding via a feeding tube is not feasible (eg, as in a patient with paralytic ileus), institute total parenteral nutrition (TPN). Restricting protein (amino acids) to 0.6 g/kg body weight per day was previously routine in the setting of hepatic encephalopathy, but this may not be necessary.

hours following acetaminophen overdose. Never administer aminoglycosides and NSAIDs, because the potential for nephrotoxicity is exaggerated greatly in this setting.

Antidotes Penicillin G (Pfizerpen)

o First DOC. Treatment of

Amanita poisoning is with IV penicillin G, although mode of action is unclear.

Silibinin (Silibinin Plus) o

Diet

Activity

o Bedrest is recommended. Medication - Antidotes that effectively bind or eliminate A phalloides toxin and toxic metabolites of acetaminophen are essential. - Acetaminophen ingestion of more than 10 g may be hepatotoxic Administering NAC permits restitution of intrahepatic glutathione. NAC is most effective when administered within 12-20

Water-soluble derivative of silymarin, which is the active ingredient in herbal preparation milk thistle. Possesses antioxidant properties that may benefit liver disease management. Activated charcoal (Actidose-Aqua, Liqui-Char, CharcoAid) o If ingestion has been recent, Amanita toxin may be bound to charcoal and absorption prevented. N-acetylcysteine (Mucomyst, Mucosil) o First DOC in acetaminophen overdose. Provides reducing equivalents to help restore depleted intrahepatic glutathione levels. Surgical Care o Liver transplantation is the definitive treatment in liver failure.

ABDOMINAL TRAUMA
Blunt Abdominal Trauma
Blunt abdominal trauma usually results from motor vehicle collisions, assaults, recreational accidents, or falls. Pathophysiology Vehicular trauma is by far the leading cause of blunt abdominal trauma in the civilian population. Auto-to-auto and auto-topedestrian collisions have been cited as causes in 50-75% of cases. Rare causes of blunt abdominal injuries include iatrogenic trauma during cardiopulmonary resuscitation, manual thrusts to clear an airway, and the Heimlich maneuver. Blunt force injuries to the abdomen can generally be explained by 3 mechanisms: o The first is when rapid deceleration causes differential movement among adjacent structures.

o The second is when intra-abdominal contents are crushed between the anterior abdominal wall and the vertebral column or posterior thoracic cage. This produces a crushing effect, to which solid viscera (eg, spleen, liver, kidneys) are especially vulnerable. o The third is external compression forces that result in a sudden and dramatic rise in o o o o o o o pain tenderness gastrointestinal hemorrhage hypovolemia Seat belt sign Abdominal distention Retroperitoneal hemorrhage: o Grey Turner sign - ecchymosis involving the flanks o Cullen sign ecchymosis involving the umbilicus

intra-abdominal pressure and culminate in rupture of a hollow viscous organ. Assessment The initial assessment of a trauma patient begins at the scene of the injury, with information provided by the patient, family, bystanders, or paramedics. The most reliable signs and symptoms in alert patients are : o Auscultation of bowel sounds in the thorax may indicate the presence of a diaphragmatic injury. o Palpation may reveal local or generalized tenderness, guarding, rigidity, or rebound tenderness, which suggests peritoneal injury. o A rectal examination should be performed to search for evidence of bony penetration resulting from a pelvic fracture o Stool should be evaluated for gross or occult blood. Other Tests Laparoscopy o Diagnostic laparoscopy has been most useful in the evaluation of possible diaphragmatic injuries, especially in penetrating thoracoabdominal injuries on the left side. Diagnostic Procedures Diagnostic peritoneal lavage o the sampling of peritoneal fluid in cases of acute pancreatitis and blunt abdominal trauma by passing a spinal needle through the abdominal wall. o The only absolute contraindication to DPL is the obvious need for laparotomy. Relative contraindications include morbid obesity, a history of multiple abdominal surgeries, and pregnancy. Management o The initial goal is to rapidly assess the patient's airway with cervical spine precautions, breathing, and circulation. This is then followed by splinting of fractures and control of external hemorrhage. o The injured patient is at risk for progressive deterioration from continued bleeding and requires rapid transport to a trauma center. o The next priority in the primary survey is an assessment of the circulatory status of the patient. Circulatory collapse in a patient with blunt abdominal trauma is

Laboratory Studies CBC count, coagulation studies, blood type, and blood cross-match (if indicated). The presence of massive hemorrhage is usually obvious from hemodynamic parameters, and the hematocrit value merely confirms the diagnosis. Urine studies include urinalysis, urine toxicologic screen, and serum or urine pregnancy tests in females of appropriate age. Amylase or lipase levels may be elevated because of pancreatic ischemia caused by the systemic hypotension that accompanies trauma. Imaging Studies Plain radiograph o The chest radiograph may aid in the diagnosis of abdominal injuries such as ruptured hemidiaphragm (eg, a nasogastric tube seen in the chest) or pneumoperitoneum. o In addition, free intraperitoneal air, or trapped retroperitoneal air from duodenal perforation, may be seen. Ultrasound o Procedure of choice in the evaluation of hemodynamically unstable trauma patients. Computed tomography o The CT scan remains the criterion standard for the detection of solid organ injuries. o CT scans, have the capability to determine the source of hemorrhage, as shown below.

usually caused by hypovolemia from hemorrhage. o Angiography is a valuable modality in the nonoperative management of adult abdominal solid organ injuries from blunt trauma. It is used aggressively for nonoperative control of hemorrhage, thus avoiding nontherapeutic cost-inefficient laparotomies. Surgical Management o Thoracotomy o Laparotomy Penetrating abdominal trauma o implies that either a GSW or a stab wound has violated the abdominal cavity. Pathophysiology o A GSW is caused by a missile propelled by combustion of powder. These wounds involve high-energy transfer and, consequently, can have an unpredictable pattern of injuries. o Stab wounds are caused by penetration of the abdominal wall by a sharp object. This type of wound generally has a more predictable pattern of organ injury. However, occult injuries can be overlooked, resulting in devastating complications. Assessment o Examination of the abdomen in a patient who is awake may indicate peritoneal signs, such as pain and guarding and rebound tenderness, which necessitate exploration without delay. o Abdominal distension in an unresponsive patient may indicate active internal bleeding that also requires exploration, especially in combination with hypotension. o Rectal examination is performed on all patients with penetrating abdominal trauma, as blood per rectum and highriding prostate can indicate bowel injury and genitourinary tract injury, respectively. o Notation of blood at the urethral meatus is also a sign of genitourinary tract injury. o Upon arrival at the emergency department, communication of the incident history and the patients vital signs to the emergency or trauma team is of paramount importance. Advanced trauma life support protocols are initiated. Airway protection and ventilatory support are followed by circulatory resuscitation with fluid infusion. Patients who present with hypotension are already in class III shock (30-40% blood volume loss), and they should receive blood products as soon as possible.

Diagnostic Findings: All patients should undergo certain basic laboratory testing, as follows: Complete blood count (CBC) provides a baseline value for later comparison, even though it may not reveal the extent of active bleeding. Basic chemistry profile (BMP) also reveals any baseline renal insufficiency or electrolyte abnormalities. Coagulation studies (PT/INR + PTT) may suggest development of coagulopathy. Arterial blood gas (ABG) provides important information regarding acid-base balance and, thus, the hemodynamic stability of the patient. Urine dipstick may reveal occult blood indicative of genitourinary tract injuries. Female patients should have urine pregnancy testing. Imaging Studies Many imaging modalities can be useful in the evaluation of a patient with penetrating abdominal trauma. Plain radiograph Chest radiograph is obtained on all patients because penetration of the chest cavity cannot be ruled out, even with abdominal stab wounds or even-numbered GSWs. Ultrasound Used to evaluate for pericardial fluid indicative of cardiac injury and for free peritoneal fluid. Free fluid in the abdomen can be a sign of hemorrhage secondary to liver or splenic laceration or, less commonly, of spillage secondary to hollow viscus injury. CT scan CT scan is used in the evaluation of patients with stab wounds to the flank and the back and in the evaluation of selected patients with abdominal stab wounds and GSWs. Rigid sigmoidoscopy Patients with blood on rectal examination who are otherwise being managed expectantly (mostly stab wounds) should undergo rigid sigmoidoscopy to rule out rectal injury. Diagnostic peritoneal lavage Diagnostic peritoneal lavage (DPL) can be performed via either a closed method (ie, small skin puncture with blind insertion of catheter over guidewire) or an open method (ie, insertion of catheter under direct vision after exposure of the peritoneum through a small infraumbilical incision). Aspiration of gross blood is positive for peritoneal penetration and organ injury. The fluid is then evaluated for the presence of red blood cells (>10,000/mm3), white blood cells (>500/mm3), bile, fibers, or particles, any of

which indicate peritoneal penetration and organ injury. Management GSWs are associated with a high incidence of intra-abdominal injuries. Nearly all patients with GSWs require laparotomy. Patients who arrive in shock should be typed and crossed for 4-8 units packed red blood cells. Nasogastric intubation o All patients undergoing endotracheal intubation require decompression of the stomach to decrease the risk of aspiration. Blood in the nasogastric tube can indicate upper gastrointestinal injury. Foley catheterization o Catheter insertion is required to monitor the fluid resuscitation status of the patient with penetrating abdominal trauma. The presence of blood in the urine is a sign of genitourinary tract injury. Tube thoracostomy o Patients with penetrating wounds to the thoracoabdominal area may require chest tube placement. Absent or significantly decreased unilateral breath sounds necessitate immediate tube thoracostomy to relieve hemothorax/pneumothorax. In other patients, hemothorax/pneumothorax will be identified on chest radiograph. Fluids should be administered rapidly. Normal saline or Ringers lactate solution can be used for crystalloid resuscitation. Patients arriving

in shock or with obvious significant bleeding should receive blood products as quickly as possible. Arterial access for continuous blood pressure monitoring is standard. Efforts should be made to limit hypothermia, including warm blankets and prewarmed fluids. Antibiotics should be administered to patients undergoing exploration.

Surgical Mangement Essential components to the trauma laparotomy include: control of bleeding, identification of injuries, control of contamination, and reconstruction (if possible). Postoperative Details Attention should be paid to: o warming the patient, o continuing fluid and blood product resuscitation, o replacing electrolytes, and o monitoring drain outputs. Complications Early postoperative complications include ongoing bleeding, coagulopathy, and abdominal compartment syndrome. The latter is treated with opening of the abdomen and temporary closure. Later complications include acute respiratory distress syndrome, pneumonia, sepsis, intra-abdominal fluid collections, wound infections, and enterocutaneous fistulae. Late complications include small bowel obstruction and incisional hernias