P
Paget’s disease
Description
Paget’s disease (osteitis deformans) is a chronic skeletal bone disorder in which there is excessive bone resorption followed by replacement of normal marrow by vascular, fibrous connective tissue and new bone that is larger, more disorganized, and weaker. Regions of the skeleton commonly affected are the pelvis, long bones, spine, ribs, sternum, and cranium. The etiology of Paget’s disease is unknown, although a viral etiology has been proposed.
Up to 40% of all patients with Paget’s disease have a relative with the disorder. Compared with women, men are affected twice as often.
Clinical manifestations
In milder forms of Paget’s disease, patients may remain free of symptoms, and the disease may be discovered incidentally on x-ray or serum chemistry findings of a high alkaline phosphatase level.
Pathologic fracture is the most common complication and may be the first indication of the disease. Other complications include osteosarcoma, osteoclastoma (giant cell tumor), or fibrosarcoma.
Diagnostic studies
Nursing and collaborative management
Management is usually limited to symptomatic and supportive care and correction of secondary deformities by either surgical intervention or braces.
■ Pain is usually managed by nonsteroidal antiinflammatory drugs (NSAIDs).
■ Orthopedic surgery for fractures, hip and knee replacements, and knee realignment may be necessary.
A firm mattress should be used to provide back support and relieve pain. The patient may be required to wear a corset or light brace to relieve back pain and provide support when in the upright position. The patient should be proficient in the correct application of such devices and know how to regularly examine areas of the skin for friction damage.
Pancreatic cancer
Description
Pancreatic cancer is the fourth leading cause of death from cancer in the United States, with the peak incidence occurring between 65 and 80 years. Most pancreatic tumors are adenocarcinomas. As the tumor grows, the common bile duct becomes obstructed and obstructive jaundice develops. Tumors starting in the body or the tail often remain silent until their growth is advanced.
The majority of cancers have metastasized at the time of diagnosis. Signs and symptoms of pancreatic cancer are often similar to those of chronic pancreatitis. The prognosis of a patient with cancer of the pancreas is poor. The majority of patients die within 5 to 12 months of the initial diagnosis, and the 5-year survival rate is less than 5%.
Pathophysiology
The cause of pancreatic cancer is unknown. Risk factors are diabetes mellitus, chronic pancreatitis, family history of pancreatic cancer, cigarette smoking, high-fat diet, and exposure to chemicals such as benzidine. Smokers are two to three times more likely to develop pancreatic cancer than nonsmokers. The risk is related to both the duration and number of cigarettes smoked.
Clinical manifestations
Manifestations include abdominal pain (dull or aching), anorexia, rapid and progressive weight loss, nausea, and jaundice.
Diagnostic studies
Collaborative care
Surgery provides the most effective treatment, but only 15% to 20% of patients have resectable tumors. The classic surgery is a radical pancreaticoduodenectomy or Whipple procedure. This procedure is a resection of the proximal pancreas (proximal pancreatectomy), the adjoining duodenum (duodenectomy), the distal portion of the stomach (partial gastrectomy), and the distal segment of the common bile duct. An anastomosis of the pancreatic duct, common bile duct, and stomach to the jejunum is done.
Nursing management
Because the patient with pancreatic cancer has many of the same problems as the patient with pancreatitis, nursing care includes the same measures (see Pancreatitis, Acute, on the facing page).
■ Psychologic support is essential, especially during times of anxiety or depression.
Pancreatitis, acute
Description
Acute pancreatitis is an acute inflammation of the pancreas, with the degree of inflammation varying from mild edema to severe hemorrhagic necrosis. It is most common in middle-aged men and women, with the rate of pancreatitis three times higher in African Americans than whites.
The severity of the disease varies according to the extent of pancreatic destruction. Some patients recover completely, others have recurring attacks, and still others develop chronic pancreatitis. Acute pancreatitis can be life threatening.
Pathophysiology
Many factors can cause injury to the pancreas. In the United States the most common cause is gallbladder disease (gallstones), which is more common in women. The second most common cause is chronic alcohol intake, which is more common in men. Smoking is an independent risk factor for acute pancreatitis. Biliary sludge, which is a mixture of cholesterol crystals and calcium salts, is found in 20% to 40% of patients with acute pancreatitis. Acute pancreatitis attacks are also associated with hypertriglyceridemia (serum levels over 1000 mg/dL).
Less common causes of acute pancreatitis include trauma (postsurgical, abdominal), viral infections (mumps, HIV), penetrating duodenal ulcers, cysts, abscesses, cystic fibrosis, certain drugs (corticosteroids, sulfonamides, nonsteroidal antiinflammatory drugs [NSAIDs]), and metabolic disorders (hyperparathyroidism, renal failure). In some cases the cause is unknown (idiopathic).
The pathophysiologic involvement of acute pancreatitis is classified as either mild pancreatitis (also known as edematous or interstitial) or severe pancreatitis (also called necrotizing pancreatitis). Patients with severe pancreatitis are at high risk for developing pancreatic necrosis, organ failure, and septic complications.
Clinical manifestations
Abdominal pain is the predominant symptom of acute pancreatitis. The pain is usually located in the left upper quadrant but may be in the mid-epigastric area. The pain commonly radiates to the back because of the retroperitoneal location of the pancreas.
Other manifestations of acute pancreatitis include nausea and vomiting, low-grade fever, leukocytosis, hypotension, tachycardia, and jaundice. Abdominal tenderness with muscle guarding is common. Bowel sounds may be decreased or absent. Paralytic ileus may occur and causes marked abdominal distention. The lungs are frequently involved, with crackles present.
Complications
Local complications of acute pancreatitis are pseudocyst and abscess.
Systemic complications of acute pancreatitis include pleural effusion, atelectasis, pneumonia, hypotension, and hypocalcemia leading to tetany.
Diagnostic studies
Collaborative care
Goals of management for acute pancreatitis include relief of pain, prevention or alleviation of shock, reduction of pancreatic secretions, correction of fluid and electrolyte imbalances, prevention or treatment of infections, and removal of the precipitating cause, if possible.
Conservative therapy is primarily focused on supportive care, including aggressive hydration, pain management, management of metabolic complications, and minimization of pancreatic stimulation. Treatment and control of pain are very important. Morphine may be used and may be combined with an antispasmodic.
It is important to reduce or suppress pancreatic enzymes to decrease stimulation of the pancreas and allow it to rest. Usually the patient is NPO, and nasogastric (NG) suction is used to reduce vomiting and prevent gastric digestive juices from entering the duodenum. Drugs that neutralize or suppress formation of HCl in the stomach, such as antacids, histamine H2-receptor antagonists, and proton pump inhibitors, also help suppress gastric acid secretion.
When the acute pancreatitis is related to gallstones, an urgent ERCP plus endoscopic sphincterotomy may be performed. This may be followed by laparoscopic cholecystectomy to reduce the potential for recurrence. Surgical intervention may be indicated when the diagnosis is uncertain and in patients who do not respond to conservative therapy. Patients with severe acute pancreatitis may require drainage of necrotic fluid collections. This can be done surgically, under CT guidance, or endoscopically. Percutaneous drainage of a pseudocyst can be performed, and a drainage tube is left in place.
Several different drugs are used to prevent and treat problems associated with pancreatitis (see Table 44-18, Lewis et al.: Medical-Surgical Nursing, ed. 9, p. 1032). Currently there are no drugs that cure pancreatitis.
Nursing management
Goals
The patient with acute pancreatitis will have relief of pain, normal fluid and electrolyte balance, minimal to no complications, and no recurrent attacks.
Nursing diagnoses
Nursing interventions
Encourage early diagnosis and treatment of biliary tract disease, such as cholelithiasis. Encourage the patient to eliminate alcohol intake, especially if there have been any previous episodes of pancreatitis.
During the acute phase, a major focus of your care is the relief of pain. Pain and restlessness can increase the metabolic rate and subsequent stimulation of pancreatic enzymes. Assess and document the duration of pain relief. Measures such as comfortable positioning, frequent changes in position, and relief of nausea and vomiting assist in reducing the restlessness that usually accompanies the pain.
Patients may require follow-up home care. Physical therapy may be needed due to loss of muscle strength. Continued care to prevent infection and detect any complications is important.
Patient and caregiver teaching
Pancreatitis, chronic
Description
Chronic pancreatitis is a continuous, prolonged, inflammatory, and fibrosing process of the pancreas. The pancreas is progressively destroyed as it is replaced by fibrotic tissue. Strictures and calcifications may also occur in the pancreas. Chronic pancreatitis may follow acute pancreatitis, but it may also occur in the absence of any history of an acute condition.
Chronic pancreatitis can be due to alcohol abuse; obstruction cause by cholelithiasis (gallstones), tumor, pseudocysts, or trauma; and systemic diseases (e.g., systemic lupus erythematosus), autoimmune pancreatitis, and cystic fibrosis.
Pathophysiology
The most common cause of obstructive pancreatitis is inflammation of the sphincter of Oddi associated with cholelithiasis (gallstones). Cancer of the ampulla of Vater, duodenum, or pancreas can also cause this type of chronic pancreatitis.
In nonobstructive pancreatitis there is inflammation and sclerosis, mainly in the head of the pancreas and around the pancreatic duct. This type of chronic pancreatitis is the most common form. In the United States, chronic pancreatitis is found almost exclusively in individuals who abuse alcohol.
Clinical manifestations
As with acute pancreatitis, a major manifestation of chronic pancreatitis is abdominal pain. The patient may have episodes of acute pain, but it usually is chronic (recurrent attacks at intervals of months or years). The attacks may become more and more frequent until they are almost constant, or they may diminish as the pancreatic fibrosis develops. The pain is located in the same areas as in acute pancreatitis but is usually described as a heavy, gnawing feeling or sometimes as burning and cramplike. The pain is not relieved with food or antacids.
Diagnostic studies
Confirming the diagnosis of chronic pancreatitis can be challenging and is based on the patient’s signs and symptoms, lab studies, and imaging.
■ Serum amylase and lipase levels may be elevated slightly or not at all.
■ Serum bilirubin and alkaline phosphatase levels may be elevated.
■ Mild leukocytosis and elevated sedimentation rate may be found.
Nursing and collaborative management
When the patient with chronic pancreatitis experiences an acute attack, the therapy is similar to that for acute pancreatitis. At other times the focus is on the prevention of further attacks, relief of pain, and control of pancreatic exocrine and endocrine insufficiency. Sometimes large, frequent doses of analgesics are needed to relieve the pain.
Patient and caregiver teaching
Parkinson’s disease
Description
Parkinson’s disease (PD) is a chronic, progressive neurodegenerative disorder characterized by slowness in the initiation and execution of movement (bradykinesia), increased muscle tone (rigidity), tremor at rest, and gait disturbance. It is the most common form of parkinsonism (a syndrome characterized by similar symptoms).
The prevalence of PD is about 160 per 100,000 people. The diagnosis of PD increases with age, with the condition affecting about 2% of people over the age of 60 years. About 15% of those diagnosed with PD are younger than 50 years old. PD is more common in men.
Approximately 20% of PD patients have a family history of PD. Many autosomal dominant and recessive genes have been linked to the development of familial PD.
Pathophysiology
Although the exact cause of PD is unknown, a complex interplay of environmental and genetic factors is involved. Between 10% and 15% of PD patients have a family history of the disease, indicating a strong genetic basis for PD. In other people, exposure to toxins or certain viruses may trigger PD.
There are many forms of parkinsonism other than PD. Parkinsonism-like symptoms have occurred after intoxication with a variety of chemicals, including carbon monoxide and manganese (among copper miners) and the product of meperidine analog synthesis, MPTP.
Drug-induced parkinsonism can follow reserpine (Serpasil), methyldopa (Aldomet), lithium, haloperidol (Haldol), and phenothiazine (Thorazine) therapy. It is also seen following the use of amphetamine and methamphetamine.
Clinical manifestations
Onset of PD is gradual and insidious, with an ongoing progression. Classic manifestations are a triad of tremor, rigidity, and bradykinesia. In the beginning stages, only a mild tremor, slight limp, or decreased arm swing may be evident. Later the patient may have a shuffling, propulsive gait with arms flexed and loss of postural reflexes. Some patients have a slight change in speech patterns.
Complications
As the disease progresses, complications may occur including motor symptoms. These include dyskinesias (spontaneous, involuntary movements), weakness, and akinesia (total immobility). Neurologic problems (e.g., dementia) and neuropsychiatric problems (e.g., depression, hallucinations, psychosis) may also occur. Dementia is present in up to 70% of patients with PD and is associated with an increase in mortality.
■ Swallowing becomes more difficult (dysphagia); malnutrition or aspiration may result.
■ General debilitation may lead to pneumonia, urinary tract infections, and skin breakdown.
Diagnostic studies
Because there is no specific diagnostic test for PD, the diagnosis is based on the history and clinical features.
Collaborative care
Because there is no cure, management is aimed at relieving symptoms.
Drug therapy
Drug therapy for PD is aimed at correcting the imbalance of central nervous system (CNS) neurotransmitters. Antiparkinsonian drugs either enhance the release or supply of DA (dopaminergic) or antagonize or block the effects of ACh in the striatum. Levodopa with carbidopa (Sinemet) is often the first drug used. Levodopa is a precursor of dopamine and can cross the blood-brain barrier. It is converted to dopamine in the basal ganglia. Prolonged use of levodopa can often result in dyskinesias and “off/on” periods when the medication will unpredictably start or stop working.
Some health care providers believe that, after a few years of therapy, the effectiveness of Sinemet wears off. Therefore they prefer to initiate therapy with a DA receptor agonist instead. These drugs include bromocriptine (Parlodel), pergolide (Permax), ropinirole (Requip), and pramipexole (Mirapex). These drugs directly stimulate DA receptors. When more moderate to severe symptoms are present, levodopa with carbidopa (Sinemet) is added to the drug regimen.
■ The antiviral agent amantadine (Symmetrel) is also an effective antiparkinsonian drug.
See Table 59-18 in Lewis et al.: Medical-Surgical Nursing, ed. 9, p. 1435, which summarizes drugs commonly used in Parkinson’s disease.
Surgical therapy
Surgical procedures are aimed at relieving symptoms of PD and are usually used in patients who are unresponsive to drug therapy or who have developed severe motor complications. Procedures fall into three categories: ablation (destruction), deep brain stimulation (DBS), and transplantation.
Transplantation of fetal neural tissue into the basal ganglia is designed to provide DA-producing cells in the brain. This form of therapy is still in experimental stages.
Nutritional therapy
Diet is of major importance because malnutrition and constipation can be serious consequences of inadequate nutrition. Patients who have dysphagia and bradykinesia need appetizing foods that are easily chewed and swallowed. The diet should contain adequate roughage and fruit to avoid constipation. Provide ample time for eating to avoid frustration.
Nursing management
Goals
The patient with PD will maximize neurologic function, maintain independence in activities of daily living for as long as possible, and optimize psychosocial well-being.
Nursing diagnoses
Nursing interventions
Promotion of physical exercise and a well-balanced diet are major concerns for nursing care. Exercise can limit the consequences of decreased mobility such as muscle atrophy, contractures, and constipation. Overall muscle tone as well as specific exercises to strengthen the muscles involved with speaking and swallowing should be included.
Because PD is a chronic degenerative disorder with no acute exacerbations, focus on teaching and nursing care directed toward the maintenance of good health, encouragement of independence, and avoidance of complications such as contractures.
Patient and caregiver teaching
■ Encourage environmental alterations, such as removing rugs and excess furniture to avoid stumbling.
■ An elevated toilet seat can facilitate getting on and off the toilet.
■ As the disease progresses, the impact on the psychologic well-being of the patient also increases. Assist the patient through listening, providing education, encouraging social interactions, and referral to the American Parkinson Disease Association (www.apdaparkinson.org).
Family caregivers (e.g., spouse, children) care for the majority of patients with PD, and as the disease progresses, the caregiver burden increases. This increase has been associated with decreases in caregiver physical and mental health. Strategies to reduce caregiver burden are described in Lewis et al.: Medical-Surgical Nursing, ed. 9, pp. 51-52.
Pelvic inflammatory disease
Description
Pelvic inflammatory disease (PID) is an infectious condition of the pelvic cavity that may involve the fallopian tubes (salpingitis), ovaries (oophoritis), and pelvic peritoneum (peritonitis). PID may be “silent” with no symptoms, whereas other women may be in acute distress. Silent PID is a major cause of infertility. PID may also be a cause of chronic pelvic pain (see Pelvic Pain, Chronic, p. 483). In the United States it is estimated that each year, 1 million women experience an acute episode of PID.
Pathophysiology
PID is often the result of untreated cervicitis. The organism infecting the cervix ascends higher into the uterus, fallopian tubes, ovaries, and peritoneal cavity. The most frequent causative organisms are Chlamydia trachomatis and Neisseria gonorrhoeae. These organisms, as well as mycoplasma, streptococci, and anaerobes, gain entrance during sexual intercourse or after pregnancy termination, pelvic surgery, or childbirth.
Clinical manifestations
Women with PID usually go to a health care provider because of lower abdominal pain.
Complications
Immediate complications of PID include septic shock and Fitz-Hugh-Curtis syndrome, which occurs when PID spreads to the liver and causes acute perihepatitis. The patient has symptoms of right upper quadrant pain, but liver function tests are normal. Tubo-ovarian abscesses may “leak” or rupture, resulting in pelvic or generalized peritonitis.
PID can cause adhesions and strictures to develop in the fallopian tubes. After one episode of PID, the risk of having an ectopic pregnancy increases 10-fold. Further damage can obstruct the fallopian tubes and cause infertility.
Diagnostic studies
A pelvic examination is used to assist in the diagnosis of PID. Women with PID have lower abdominal tenderness, bilateral adnexal tenderness, and positive cervical motion tenderness.
■ Diagnostic criteria may also include fever and abnormal vaginal or cervical discharge.
■ Cultures for gonorrhea and chlamydia are also obtained.
■ A pregnancy test is done to rule out ectopic pregnancy.
Collaborative care
Treatment of PID is usually on an outpatient basis. The patient is given a combination of antibiotics such as cefoxitin (Mefoxin) and doxycycline (Vibramycin) to provide broad coverage against the causative organisms. The patient must not have intercourse for 3 weeks. Her partner(s) must be examined and treated. Physical rest and oral fluids are also important. Reevaluation in 48 to 72 hours, even if symptoms are improving, is essential.
If outpatient treatment is not successful or the patient is acutely ill or in severe pain, hospital admission is indicated. Maximum doses of parenteral antibiotics are then given with analgesics to relieve pain and IV fluids to prevent dehydration. Corticosteroids may be added to the antibiotic regimen to reduce inflammation. Application of heat to the lower abdomen or sitz baths may be used to improve circulation and decrease pain. Bed rest in semi-Fowler’s position promotes pelvic cavity drainage and may prevent the development of abscesses.
An indication for surgery is the presence of abscesses that fail to resolve with IV antibiotics. The abscesses may be drained by laparotomy or laparoscopy. Childbearing function in young women is preserved whenever possible.
Nursing management
Prevention, early recognition, and prompt treatment of vaginal and cervical infections can help prevent PID and its serious complications. Provide information regarding factors that place a woman at increased risk for PID. Urge women to seek medical attention for any unusual vaginal discharge or possible infection of their reproductive organs.
During hospitalization for PID, you have an important role in implementing drug therapy, monitoring the patient’s health status, and providing symptom relief and patient teaching. Explain the need for limited activity, being in a semi-Fowler’s position, and increased fluid intake. Assess the degree of abdominal pain to provide information about the effectiveness of drug therapy.
Pelvic pain, chronic
Description
Chronic pelvic pain refers to pain in the pelvic region (below the umbilicus and between the hips) that lasts 6 months or longer. It accounts for 10% of all visits to gynecologists and is the reason for 20% to 30% of all laparoscopies. Up to one third of women who have pelvic inflammatory disease (PID) have chronic pelvic pain. The cause of chronic pelvic pain is often hard to find.
Manifestations and diagnostic studies
Manifestations of chronic pelvic pain include severe and steady pain, intermittent pain, dull and achy pain, pelvic pressure or heaviness, and sharp pains or cramping. Pain during intercourse or while having a bowel movement may also occur.
Collaborative care
If the cause of chronic pelvic pain is found, such as PID, treatment focuses on that cause (see Pelvic Inflammatory Disease, p. 480). If an infection is the source of the problem, antibiotics will be used. If no cause can be found, treatment focuses on managing the pain. Over-the-counter pain medications (e.g., aspirin, ibuprofen, acetaminophen) may provide some relief. Sometimes stronger pain drugs may be needed. Birth control pills or other hormonal medications may help relieve cyclic pelvic pain related to menstrual cycles.
Tricyclic antidepressants (e.g., amitriptyline [Elavil], nortriptyline [Pamelor]) have pain-relieving as well as antidepressant effects. These drugs may help improve pain even in women who do not have depression. The patient may be encouraged to get counseling for any emotional issues.
Laparoscopic surgery may be used to remove pelvic adhesions or endometrial tissue. As a last attempt at treatment, a hysterectomy may be done.
Peptic ulcer disease
Description
Peptic ulcer disease is an erosion of the mucosa resulting from the digestive action of hydrochloric acid (HCl) and pepsin. Any portion of the GI tract that comes into contact with gastric secretions is susceptible to ulcer development, including the lower esophagus, stomach, and duodenum, and at the margin of a gastrojejunal anastomosis site after surgical procedures. Approximately 350,000 new cases of ulcers are diagnosed each year.
Peptic ulcers can be classified as acute or chronic, depending on the degree and duration of mucosal involvement, and gastric or duodenal, according to the location.
■ Gastric and duodenal ulcers, although defined as peptic ulcers, are distinctly different in etiology and incidence (Table 66). Generally, the treatment of all ulcer types is similar.
Table 66
Comparison of Gastric and Duodenal Ulcers
| Gastric Ulcers | Duodenal Ulcers | |
| Lesion | Superficial, smooth margins. Round, oval, or cone shaped. | Penetrating (associated with deformity of duodenal bulb from healing of recurrent ulcers). |
| Location of lesion | Predominantly antrum; also in body and fundus of stomach. | First 1-2 cm of duodenum. |
| Gastric secretion | Normal to decreased. | Increased. |
| Incidence | Greater in women. | Greater in men, but increasing in women (especially postmenopausal). |
| Peak age 50-60 yr. | Peak age 35-45 yr. | |
| More common in people of lower socioeconomic status. | Associated with psychologic stress. | |
| With smoking, drug use (aspirin, NSAID), and alcohol use, | With smoking, drug use, and alcohol use. | |
| With incompetent pyloric sphincter and bile reflux. | Associated with other diseases (e.g., chronic obstructive pulmonary disease, pancreatic disease, hyperparathyroidism, Zollinger-Ellison syndrome, chronic renal failure). | |
| Clinical manifestations | Burning or gaseous pressure in high left epigastrium and back and upper abdomen. | Burning, cramping, pressure-like pain across midepigastrium and upper abdomen. Back pain with posterior ulcers. |
| Pain 1-2 hr after meals. If penetrating ulcer, aggravation of discomfort with food. | Pain 2-4 hr after meals and midmorning, midafternoon, middle of night. Periodic and episodic. Pain relief with antacids and food. | |
| Occasional nausea and vomiting, weight loss. | Occasional nausea and vomiting. | |
| Recurrence rate | High. | High. |
| Complications | Hemorrhage, perforation, gastric outlet obstruction, intractability. | Hemorrhage, perforation, obstruction. |
Pathophysiology
Peptic ulcers develop only in the presence of an acid environment. The back-diffusion of HCl into the gastric mucosa results in cellular destruction and inflammation. Histamine is released from the damaged mucosa, resulting in vasodilation and increased capillary permeability and further secretion of acid and pepsin. A variety of agents are known to destroy the mucosal barrier (see Gastritis, p. 241).
In addition to chronic gastritis, Helicobacter pylori is associated with peptic ulcer development. Approximately two thirds of the world’s population is infected with H. pylori. In the stomach the bacteria can live a long time by colonizing the gastric epithelial cells within the mucosal layer. The bacteria also produce urease, which metabolizes urea-producing ammonium chloride and other damaging chemicals. Urease also activates the immune response with both antibody production and the release of inflammatory cytokines.
Clinical manifestations
Discomfort generally associated with gastric ulcer is located high in the epigastrium and occurs about 1 to 2 hours after meals. The pain is described as burning or gaseous. If the ulcer has eroded through the gastric mucosa, food tends to aggravate rather than alleviate the pain.
Duodenal ulcer symptoms occur when gastric acid comes in contact with the ulcer, generally 2 to 5 hours after a meal. The pain is described as “burning” or “cramplike.” It is most often located in the midepigastric region beneath the xiphoid process. Duodenal ulcers can also produce back pain. A characteristic of duodenal ulcer is its tendency to occur continuously for a few weeks or months and then disappear for a time, only to recur some months later.
Complications
Major complications of peptic ulcers are hemorrhage, perforation, and gastric outlet obstruction. All are considered emergency situations and may require surgical intervention.
Hemorrhage is the most common complication. Duodenal ulcers account for a greater percentage of upper GI bleeding than gastric ulcers.
Perforation, the most lethal complication, occurs when the ulcer penetrates the serosal surface with spillage of either gastric or duodenal contents into the peritoneal cavity. The contents entering the peritoneal cavity from the stomach or the duodenum may contain saliva, food particles, HCl acid, pepsin, bacteria, bile, and pancreatic enzymes. Bacterial peritonitis may occur within 6 to 12 hours.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
