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This paper describes a case of acute pancreatitis occurring in a patient immediately after delivery and in primigravida. The patient had a family case history of dyslipidemia (Type IV). The pregnancy had been complicated by preeclampsia treated at home with nifedipine tablets (one tablet three times a day) with good results on pressure values; lipidic values were high despite dietary measures taken. The baby at birth weighed 3830 g after physiologic labour and a natural delivery. Acute pancreatitis was diagnosed after observation of epigastralgia with irradiation on the left shoulder, vomiting, symptoms of acute abdomen such as sweating, increased pulse rate, hypotension, abdominal pain on palpation, and absence of peristalsis. An analysis of the blood showed high levels of amylase and hyperglycemia, an increase in XDP, and leucocytosis. Instrumental tests such as pancreatic echography revealed an increase in pancreatic volume, uneven structure of the parenchyma and higher levels of liquid in the peritoneum. The patient was moved to intensive-care, a nasal gastric probe inserted, hydroelectrolytic treatment was begun, vital functions monitored, pain kept under control by medical therapy, and antibiotics administered. Subsequent tests showed an improvement in the parameters of pancreatic functions (amylase, lipase, calcium hematic) and their gradual return to normal values. The computerized tomography of abdomen additionally revealed the presence of pancreatic pseudo-cysts and effusion of peritoneal liquid near the right kidney. The patient was discharged after two weeks in the surgical ward. There are many caused of acute abdomen during and immediately after pregnancy, and one of these is acute pancreatitis, though rare (occurring between 1:3800 and 11.467 according to Rabkin).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute pancreatitis in pregnancy]. 835 Oct 66

A 18 month-old boy with asplenic syndrome was admitted to our hospital with a twelve hours history of mucous vomiting, abdominal pain and a round epigastric mass. It was diagnosed as having a gastric volvulus and an emergency laparotomy was performed. The stomach was situated at the right side and a mesenterioaxial volvulus was found, with cyanosis of the antrum. The gastrophrenic and gastrosplenic ligaments were absent. The clinical and radiological characteristics of asplenic syndrome are reviewed. The pediatric surgeons must be aware of the digestive malformations of the asplenic syndrome, because some of that like malfixation of the stomach could be the cause of an acute abdomen.
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PMID:[Acute gastric volvulus in a patient with asplenic syndrome]. 849 38

A 9-year-old girl presented with severe intermittent upper abdominal pain and bilious vomiting for 1 day. Abdominal echography demonstrated severe distension of the gallbladder with marked change in its long axis. Torsion of the gallbladder was suspected preoperatively. Counter-clockwise rotation of the gallbladder around its neck for more than 180 degrees with necrosis of the whole gallbladder was found during the emergency laparotomy. Choleystectomy was performed smoothly after detorsion of the gallbladder. The postoperative recovery was uneventful. Although torsion of the gallbladder is rarely reported in children, we should keep this possibility in mind as a differential diagnosis of acute abdomen.
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PMID:[Torsion of gallbladder in childhood: a case report]. 852 44

Postemetic spontaneous rupture of the esophagus is an intrathoracic disaster which is generally lethal if untreated. The tragedy seems to strike more often than commonly suspected. The current literature review focuses on publications since 1980 and includes the retrospective review of 18 additional patients treated in our hospital for spontaneous rupture of the esophagus. Frequently, a wide variety of unspecific symptoms has led to the mistaken diagnosis of an acute abdomen, pancreatitis or cardiac arrest. About 40% of the patients with spontaneous rupture of the esophagus presented a history of alcoholism or heavy drinking and 41% suffered from gastroduodenal ulcer disease. Pain (83%) and vomiting (79%) often associated with dyspnea (39%) and shock (32%) are the major symptoms. This unspecific symptomatology delayed the correct diagnosis of the Boerhaave's syndrome and resulted in a significant complication rate. The mortality rate associated with Boerhaave's syndrome was 50% from the first successful surgical repair in 1947 by Barrett to 1980. After 1980, however, the mortality rate dropped to 31%, because of earlier diagnosis, surgical repair and improvement in intensive care. When surgery is delayed, the prognosis of patients with spontaneous rupture of the esophagus is in general severe.
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PMID:Boerhaave's syndrome: analysis of the literature and report of 18 new cases. 907 78

A 31-year-old pregnant woman who was an active cocaine abuser presented to our emergency department five times in 1 week for abdominal pain and vomiting. She continued to use cocaine regularly despite having abdominal pain. Her fifth admission was for seizures. There were no objective signs of peritoneal inflammation and the rectal guiac examination was repeatedly negative. The patient progressed to severe septic shock. Intraabdominal sepsis and/or bowel perforation was suspected. Exploratory laporatomy revealed gangrene and perforation of the small intestine and fecal peritonitis. She rapidly developed multiorgan failure and died. Gastrointestinal complications resulting from cocaine use are uncommon. Our case is unique in that the patient was pregnant, used cocaine by the intranasal route, and lacked objective signs of acute abdomen. Emergency physicians should be aware of the morbidity associated with the use of cocaine.
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PMID:Cocaine-associated intestinal gangrene in a pregnant woman. 927 Mar 93

The syndrome of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is an uncommon neuromuscular disorder caused by mitochondrial dysfunctions that result in headaches, seizures, and progressive dementia. The authors describe a clinical case study of gastrointestinal manifestations in a pedigree with MELAS, in which all three children, ages 11, 8, and 6, demonstrated acute onset of intestinal obstruction. They unexpectedly showed severe abdominal distension and vomiting. Their parents had no clinical manifestation. The first female sibling underwent an emergent laparotomy because she was diagnosed to have intestinal strangulation. She had postoperative complications caused by progressive lactic acidosis and died the next day. The second and third sisters had similar onsets of the disease and were treated with gastrointestinal decompression and intravenous administration of lactate-free fluid and coenzyme Q10. Genetic testing using blood samples showed an A-to-G point mutation at nucleotide position 3243 in the tRNALeu(UUR) region in the mitochondrial DNA. In MELAS children who demonstrate acute onset of gastrointestinal manifestations, a careful review of family history and an elevation of serum lactate and pyruvate levels may enable a differential diagnosis to be made of acute abdomen to avoid unnecessary surgical intervention.
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PMID:Familial occurrence of intestinal obstruction in children with the syndrome of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS). 986 67

The appendicitis is the commonest cause of an acute abdomen in children older 1 year of age. Only 5% of children with appendicitis are younger than 2 years of age. There is a familial preponderance. The younger the child the faster the symptoms of the disease are increasing in intensity. The symptoms starts with unspecific periumbilical or epigastric pain, followed by nausea, vomiting and restlessness at night. Finally the pain moves to the position of the appendix. The position of the appendix shows a high variation in children thus the pain characteristic is not uniform. Laboratory tests are not reliable but ultrasonography is recommended to exclude other diseases and to try to confirm the diagnoses. With the technique of "Graded compression Sonography" the rate of non identified appendicitis has been reduced under 5%. Laparoscopy is another option. Its use just for diagnostic purposes is limited but is recommended widely for primary therapeutic treatment with laparoscopic performed appendectomy. Laparoscopy has a special advantage against conventional appendectomy in the diagnostic of recurrent unspecific abdominal pain in children and in cases with interval appendectomy. Finally in pseudoappendicitis and pseudoperitonitis in children with immunvasculitis and other extraabdominal diseases. Letality of the acute appendicitis is zero.
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PMID:[Acute appendicitis in the child]. 988 Aug 78

A child is said to have an 'acute abdomen' in case of severe abdominal pain of sudden onset. Further investigations are necessary if the pain is very bad, persists for longer than 3-4 hours or is accompanied by vomiting. Failure to make the correct diagnosis may result in severe complications. The principal cause in an older child is acute appendicitis. This diagnosis is to be based on the anamnesis, physical examination and laboratory tests. If one of these is typical, active observation is indicated; if two or three are typical, appendectomy is indicated. Differential diagnoses can only be made during laparotomy. Intussusception occurs more frequently in toddlers. In a child with possible intussusception, observation is not justified: the diagnosis should be excluded by a contrast colonic X-ray, or operation should be performed either immediately or, if the symptoms persist, after the X-ray. Rest and patience, careful and child-adapted approach, and correct evaluation of aberrant symptoms may minimize unnecessary intervention.
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PMID:['Acute abdomen' in children]. 1008 38

Visceral pain is caused by either distension or contraction of the visceral muscular wall or obstruction of hollow gastrointestinal organs. Unlike the somatic pain due to peritonitis, visceral pain is diffuse, epigastric, periumbilical and is often accompanied by nausea, vomiting and restlessness. We demonstrate the significance of visceral pain in the differential diagnosis of the acute abdomen presenting five cases of appendicitis and cholecystitis. A correct early diagnosis of the acute abdomen while signs of local peritonitis are still absent (appendicitis in atypical location, recurrent acute appendicitis, spontaneous reopening of an occlusion) is facilitated by the awareness for the characteristics and symptoms of visceral pain, and therefore careful taking of the patient's history. A history lacking visceral pain on the other hand represents an important clue for the diagnosis of other conditions (gynecological, diverticulititis, etc.) with acute pelvic peritonitis.
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PMID:[Visceral pain in acute abdomen]. 1032 Nov 25

There are three clinical presentations of anthrax in humans: cutaneous (>95% of cases), orogastric and inhalational. The infectious form, the spore, enters the body and is thought to germinate within macrophages either at the site of inoculation (cutaneous or orogastric) or in the regional lymph node (inhalational). The bacillus then synthesizes its antiphagocytic capsule and the lethal and oedema toxins which interfere with the non-specific host defences leading to the characteristic locally destructive lesion and spread by lymphatics to the systemic circulation and other organs. The cutaneous form begins as a papule which progresses over several days to a vesicle and then ulcerates. There is often oedema, sometimes massive, probably due to the oedema toxin that surrounds the lesions which then develop a characteristic black eschar. The patient may be febrile with mild to severe systemic symptoms of malaise, headache and toxicity. Oropharyngeal anthrax presents with severe sore throat or an ulcer in the oropharyngeal cavity associated with neck swelling, fever, toxicity and dysphagia. Gastrointestinal anthrax begins with anorexia, nausea, vomiting and abdominal pain which may be similar to an acute abdomen. There may be diarrhoea and ascites, both of which may be haemorrhagic. Inhalational anthrax begins with non-specific symptoms of malaise, fever, myalgia and non-productive cough. After a period of 2-3 days, this is followed by a sudden onset of severe respiratory distress associated with diaphoresis, cyanosis and increased chest pain. There may be a widened mediastinum and pleural effusions on chest X-ray. Death follows in 24-36 h from respiratory failure, sepsis and shock. The diagnosis of anthrax is easy if it is considered. The organism is readily observed by Gram or Wright stain in local lesions or blood smear and can be easily cultured from the blood and other body fluids. However, because of its rarity, it is not often included in the differential diagnosis and in inhalational disease the diagnosis is rarely made until the patient is moribund. More rapid diagnostic tests are under development. Penicillin, combined with supportive care, remains the mainstay of treatment, although the organism is susceptible in vitro to many antibiotics. In recent years, there have been significant advances in our knowledge of the organism and its toxins and it is anticipated that similar progress will be made in the future in developing more rapid diagnostic tests and new modalities of treatment.
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PMID:Clinical aspects, diagnosis and treatment of anthrax 1047 74


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