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Serum sickness

Serum sickness is a reaction to an antiserum derived from an animal source. It is a type of hypersensitivity, specifically immune complex hypersensitivity. Serum sickness typically develops up to ten days after exposure to the antiserum, and symptoms are similar to an allergic reaction. However, it is different to anaphylaxis, since the symptoms are not instantaneous. more...

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Causes

Serum sickness can be developed as a result of exposure to antibodies derived from animals. These serums are generally administered in order to prevent infection. When the antiserum is given, the human immune system can mistake the proteins present for harmful antigens. The body produces antibodies, which combine with these proteins to form immune complexes. These complexes can cause more reactions, and cause the symptoms detailed below. Serum sickness can also be caused by several drugs, notably penicillin based medicines.

Symptoms

Symptoms can take as long as fourteen days after exposure to appear, and may include:

  • Rashes
  • Joint Pain
  • Fever
  • Lymph node swelling
  • Shock
  • Decreased blood pressure

Treatment

Symptoms will generally disappear on their own, although corticosteroids may be prescribed in the most severe forms. Antihistamine may also be used.

Read more at Wikipedia.org


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An unusual case of travel sickness - roentgenogram of the month
From CHEST, 10/1/03 by Julian J. Leggett

A 28-year-old man presented with increasing shortness of breath, He described a 5-month history of intermittent abdominal pain and weight loss. This had followed a brief illness during a boisterous summer holiday in the Balearic Islands, which had been characterized by nausea and a short-lived, vague abdominal pain. He was a smoker of 12 pack-years and denied excessive alcohol intake. A chest radiograph was performed (Fig 1). Following a diagnostic pleurocentesis and after insertion of an intercostal drain, a CT scan of the chest was obtained (Fig 2).

[FIGURES 1-2 OMITTED]

Laboratory Results

The findings of the examinations were as follows: hemoglobin level, 9.82 g/dL; platelet count, 1,050 x [10.sup.9] cells/L; leukocyte count, 4.9 x [10.sup.9] cells/L; erythrocyte sedimentation rate, 11 mm/h; C-reactive protein level, 65.7 rag/L; serum amylase level, normal; liver function test results, normal; albumin level, 23 g/L; exudative pleural effusion protein level, 35 g/dL; glucose level, 5.7 retool/L; pH, 7.73; WBC count, 22 cells/[micro]L (50% lymphocytes/50% polymorphs); and RBC count, 72 cells/[micro]L.

Diagnosis: Intrapleural and mediastinal pseudocysts complicating chronic pancreatitis

Figure 1 shows a loculated hydropneumothorax involving the left hemithorax with a contralateral deviation of the mediastinum. High levels of pancreatic enzymes in the pleural fluid (7,880 U/L; normal range, 30 to 110 U/L) confirmed the presence of pancreatic pseudocysts within the pleural cavity.

The results of initial ultrasound imaging of the abdomen indicated a normal pancreas. Figure 2 shows an axial CT scan slice through the lower chest at the level of the left atrium following chest drain insertion. It illustrates a moderate pericardial effusion. There is a cystic mass in the posterior mediastinum as well as bilateral pleural effusions. The patient was treated with intercostal chest drainage but continued to have an output of 1,000 to 1,500 mL daily after apparent resolution of the initial effusion, IV somatostatin was initiated in an attempt to limit pancreatic exocrine timction. Total parenteral nutrition (TPN) was required for a prolonged period to improve nutritional status in the face of a relative hypercatabolic state.

CT scanning of the chest and abdomen indicated the successful resolution of the pleural effusion but revealed a pseudocyst in the tail of the pancreas (Fig 3, top) passing posterior to the liver through the diaphragmatic hiatus and into the posterior mediastinum (Fig 3, bottom). The pericardial effusion was drained using a catheter, but, due to the inaccessibility of the mediastinal pseudocyst, a CT-guided radiologic drain was inserted transhepatically, and 600 mL purulent fluid was drained. The patient was discharged from the hospital after a significant period of convalescence.

[FIGURE 3 OMITTED]

DISCUSSION

We have described a patient who developed intrapleural and mediastinal pseudocysts as a consequence of chronic pancreatitis. In this case, the initial episode of acute pancreatitis was mild and difficult for the patient to recollect. There was no evidence radiologically of gallstones, and alcohol consumption was allegedly within recommended guidelines. The pseudocyst connected to the pleural cavity through the diaphragmatic hiatus, a recognized but uncommon presentation in patients with chronic pancreatitis. Few cases of mediastinal pseudocysts have been reported in the literature. Fluid collecting in or around an acutely inflamed pancreas can persist for 4 to 6 weeks and can become encapsulated. Such pseudocyts are found in approximately 25% of patients with chronic pancreatitis.

Pleural effusions can occur in patients with acute pancreatitis. One study found pleural effusions in 20% of patients, and pericardial effusions in 17%. (1) The presence of pleural effusions was thought to be an accurate predictor of severity, and all effusions were associated with an increased risk of subsequent pseudocyst development. (1)

Left ventricular function has been shown to be normal in those patients with pericardial effusions, and their presence appears to be unrelated to the severity of the illness. (2) The traditional thinking was that a psendocyst measuring > 5 cm in diameter, that had been present for [greater than or equal to] 6 weeks, should be surgically excised. Studies have suggested that the size should be monitored with ultrasonography and that therapy should be commenced if and when symptoms dictate. (3)

Conservative treatment for pseudocyst resolution includes TPN and somatostatin injections. The treatment of acute pseudocysts with TPN has shown that the majority of patients have clinical and radiologic regression of the pseudocysts, although a significant proportion experience catheter-related complications. (4) Cystogastrostomy or cystoduodenostomy are associated with lower perioperative complications and can negate the need for pancreatectomy. Percutaneous catheter drainage is also effective. Endoscopic procedures also can be used for pancreatic pseudocyst decompression and are gaining popularity. (5)

Pancreatic pseudocysts may connect to the pleural cavity via a pancreatic-pleural fistula, although sometimes a connection cannot be identified with contrast imaging. Other atypical sites include the liver, spleen, stomach wall, and mediastinum. Natural pathways for their development include the hepatoduodenal, gastrohepatic, and gastrosplenic ligaments. (6)

Chronic pancreatitis may present with vague symptoms, and an analysis of pleural fluid for amylase is essential in making a quick diagnosis. The extension of extrapancreatic fluid into the mediastinum is a rare occurrence and, if present, is best defined radiologically by CT scanning. (7)

REFERENCES

(1) Maringhini A, Ciambra M, Patti R, et al. Ascites, pleural, and pericardial effusions in acute pancreatitis: a prospective study of incidence, natural history and prognostic role. Dig Dis Sci 1996; 41:848-852

(2) Pezzilli R, Billi P, Bertaccini B, et al. Pericardial effusion and left ventricular function in acute pancreatitis. Am J Gastroenterol 1996; 91:997-1000

(3) Balthazar EJ, Freeny PC, van Sonnenberg E. Imaging and intervention in acute pancreatitis. Radiology 1994; 193: 297-306

(4) Sharudin MD, Noori SM. Pancreatic pseudocyst: the controversial value of total parenteral nutrition. Hepatogastroenterology 1997; 44:559-563

(5) Lawson JM. Bailie J. Endoscopic therapy for pancreatic pseudocysts. Gastrointest Endosc Clin N Am 1995; 5:181-193

(6) Hamm B, Franzan N. A typically located pancreatic pseudocysts in the liver, spleen, stomach wall and mediastinum: their CT diagnosis. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Vertfahr 1993; 159:522-527

(7) Owens GR, Arger PH, Mulhern CB, et al. CT evaluation of mediastinal pseudocyst. J Comput Assist Tomogr 1980: 4:256-.959

* From the Departments of Respiratory Medicine (Drs. Leggett, Mainie and Convery) Surgery (Mr Mackle) and Radiology Dr McAteer), Craigavon Area Hospital, Portadown, Northern Ireland.

Received January 29, 2002; revision accepted April 26, 2002. Correspondence to: Julian J. Leggett, 26 Ravensdene Park, Belfast BT6 0DA, Northern Ireland; e-mail: jjleggett@hotmail.com

COPYRIGHT 2003 American College of Chest Physicians
COPYRIGHT 2003 Gale Group

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