Acute pancreatitis after translumbar aortography.
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Biomedical subjects
Publications and source records attributed to C W Imrie.
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In 502 fibreoptic oesophagogastroduodenoscopies performed over 30 months, 14 cases (2.8%) of symptomatic duodenitis without an associated duodenal ulcer were diagnosed. Follow up (1 to 3-5 years) including repeat endoscopy and double-contrast barium meal showed that duodenal ulcers later developed in 6 patients. All have undergone surgery. A further 2 patients continued to complain of dyspepsis, and repeat endoscopy showed duodenitis, confirmed by conventional light microscopy (haematoxylin and eosin). The remaining patients are symptom-free. Repeat endoscopy and histological examination were either normal or showed mild inflammation of the duodenal mucosa. These findings suggest that duodenitis can cause symptoms and may be part of the pathophysiological spectrum of duodenal ulceration rather than a separate disease. It may represent both the production and healing phases of duodenal ulceration.
Severe arterial hypoxia while breathing ambient air (Pao2 less than 60 mm Hg) was recorded in 38 (45 per cent) of a group of 84 patients with acute pancreatitis when arterial blood gas monitoring was performed during the first week of illness. This contrasted with an incidence of 19 per cent severe hypoxia in a heterogeneous group of 68 patients with acute abdominal pain admitted as surgical emergencies. Clinical evidence of respiratory embarrassment was rarely present in either the patients with acute pancreatitis or the other patients. Arterial hypoxia was related to the prognosis in both groups. It is recommended that all patients with acute pancreatitis have routine arterial blood gas monitoring performed during the first 5 days of illness. Furthermore, all older patients (over 60 years) and younger patients with moderate hypoxia (Pao2 less than 70 mm Hg) should be given supplementary humidified oxygen. An awareness of occult respiratory insufficiency in surgical emergency admissions, and especially in acute pancreatitis, is of importance.
Measurement of serum ionized calcium was performed daily for 7 days after admission in 8 consecutive patients with acute pancreatitis. The results support the findings of our previous study that the most common cause of the low serum calcium often found in patients with this disease is a low serum albumin; when correction of serum calcium is made for hypo-albuminanemia, most patients are found to be normocalcaemic. The occasional hypocalcaemia as shown by the 'corrected' serum calcium or by serum ionized calcium measurement is usually mild and transient, indicating that the normal homoeostatic mechanisms of the body can efficiently maintain the physiologically active fraction of the serum calcium within, or close to, the normal range. These findings explain the rarity of overt and subclinical tetany in acute pancreatitis. This study has shown that correction of serum calcium for albumin provides similar information to the direct measurement of serum ionized calcium. The value of 'apparent' hypocalcemia in assessing severity of acute pancreatitis requires reappraisal, while greater attention should be directed towards the investigation and management of hypoalbuminaemia in this disease.
Endoscopic retrograde choledochopancreatography (ERCP) was employed in 52 patients symptomatic after cholecystectomy in whom barium meal studies and intravenous cholangiography had failed to yield a diagnosis. Cannulation of the papilla of Vater was carried out in 50 of the patients in a mean time of 10 min. Diagnostic information demonstrating a pathological lesion or a normal biliary and pancreatic ductal system was obtained by means of endoscopy and ERCP in 48 cases. There were no serious complications. A pathological lesion was demonstrated in all but one of the patients presenting with jaundice, cholangitis or pancreatitis but the diagnostic yield was not as high in patients with vague upper abdominal symptoms. Endoscopy and ERCP are the investigative procedures of first choice in complex post-cholecystectomy cases in whom intravenous cholangiography fails, gives incomplete information or suggests normality in the face of continuing symptoms or clinical evidence of residual biliary disease.
A prospective study of 116 patients with acute pancreatitis included routine screening for evidence of viral infection. Five patients (all female) exhibited significant rising antibody titres to Coxsackie B or mumpsvirus, while none of the remaining 111 patients did. Diarrhoea was a prodromal feature of the pancreatitis in those patients with evidence of viral disease. Screening patients with acute pancreatitis for Coxsackie B and mumpsvirus infections is worthwhile in the identification of aetiological factors and may minimise protracted biliary investigations. The incidence of "idiopathic" acute pancreatitis in this study was 5-2% (six patients).
Twenty-five patients with acute pancreatitis were studied prospectively in the first week of their admission using haematological and coagulation tests. Platelet counts initially fell and later returned to admission levels. Rising levels of plasma fibrinogen were recorded. The kaolin cephalin clotting time was shorter than its control in twenty-one patients. Eighteen patients had elevated fibrinogen degradation products and fourteen had a positive ethanol gelation test. It is suggested that by taking into account the results in series of individual patients a degree of intravascular coagulation may be a common feature of acute pancreatitis. In one patient (presented in detail) strong evidence for disseminated intravascular coagulation was found
Twenty-six patients with acute pancreatitis and normal chest radiographs on admission were studied. Twelve (46%) developed abnormalities in the first five days of illness. Twenty-four of the 25 patients tested developed an arterial pO2 of less than 10.6 kPa (80 mmHg) but severe hypoxia was present in a greater percentage of patients whose chest radiology became abnormal. Blood gases and chest radiographs should be checked on a regular basis in patients with acute pancreatitis.
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Hypoalbuminaemia has been consistently observed in a prospective study of 130 patients with acute pancreatitis. A study was initiated, therefore, to find out if the hypocalcaemia of acute pancreatitis could be explained by the associated hypoalbuminaemia. 64.4% of all serum calcium results were in the apparently hypocalcaemic range. A comparable incidence of hypoalbuminaemia was observed. The 'uncorrected' total serum calcium and serum albumin showed a similar pattern in their daily changes and also a significant correlation overall. When correction of serum calcium was made for albumin levels, only 10.9% of all results represented varying degrees of 'true' hypocalcaemia. Mortality and severity of acute pancreatitis related as closely to hypoalbuminaemia as to uncorrected hypocalcaemia. It is concluded that a low serum albumin should be regarded as the most common cause of a low serum calcium in acute pancreatitis. Routine albumin administration is proposed, a procedure which has been shown to be associated with improved mortality rate and morbidity in this disease.
Thirty-eight patients have been examined by ultrasound when symptoms or sign suggested the development of a pseudocyst following an attack of proven acute pancreatitis. Pseudocyst was diagnosed in 23 of the 38 cases. Five patients had multilocular cysts, four of which were shown to be communicating. Laparotomy was carried out on 14 of the 23 patients and surgical drainage was performed in 12 cases. The remaining nine cases were monitored and showed steady regression. Small cysts arising in the head of pancreas may give rise to recurrent or persistent pancreatitis and may be demonstrated pre-operatively by ultrasound but not readily by other means. A further 12 patients showed an area of irregular absorption of ultrasound interpreted as an inflammatory mass. Monitoring of these cases showed progressive resolution without cyst formation. Three of these cases subsequently required laparotomy-one developed an abscess and one necrosis of the body and tail of pancreas while a third developed severe pancreatic fibrosis of the area identified by ultrasound. The ability to distinguish between pseudocysts and inflammatory masses and to demonstrate communication between multiple cysts is of considerable value in pre-operative diagnosis.
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