Pancreatitis is inflammation of the pancreas. Acute and chronic pan­creatitis are differentiated.

ACUTE PANCREATITIS

Aetiology andpathogenesis. Most often there exists connection between acute pancreatitis and inflammation of bile ducts, cholelithiasis in particular. This connection is explained by possible penetration of bile (usually infected) into the pancreatic duct and activation of the en­zymes (trypsin and lipase) of the pancreatic juice. This condition can arise when the common bile duct and the pancreatic duct have a common ampulla, e.g. in spasm of the sphincter of the hepatopancreatic ampulla, obstruction of the ampulla by a stone, increased pressure in the duodenum (during coughing, vomiting, etc). Upset outflow of the pancreatic juice in obstruc­tion of the duct by a stone, oedema of the duct mucosa, etc. is also important.

Among the other aetiological factors are alcoholism, poisoning with chemicals, such as lead, cobalt, phosphorus, arsenic, etc., and alimentary disorders (overeating or inadequate nutrition), certain infectious diseases (e.g. epidemic parotitis, virus hepatitis), local cir­culatory disorders in the pancreas due to spasms of the vessels, embolisms and thrombosis arising due to general changes in the vascular system.

Activation of proteolytic enzymes in the pancreas is important in the pathogenesis of pan­creatitis irrespective of its aetiology. This causes enzymatic digestion (autolysis) of the pan­creatic parenchyma with haemorrhages and fat necrosis. The developmental mechanisms of pancreatitis depend also on secondary infection of the excretory ducts that develops by ascen­ding haematogenic or (less frequently) lymphogenic routes.

Pathological anatomy. Inflammation, necrosis, and in later periods atrophy, fibrosis and calcification of the pancreas are revealed. Abscesses of variable size are found in purulent in­flammation of the pancreas, or diffuse melting of the pancreatic tissue develops with subse­quent fibrosis of the pancreas (in favourable outcome). Mild forms of pancreatitis are only manifested by inflammatory oedema of the gland.

Clinical picture. Acute pancreatitis occurs mostly in women with disordered fat metabolism (aged 30 to 60). The disease usually begins by a sudden pain in the upper abdomen which arises after taking ample and fat food or alcohol. In mild cases the pain is not severe and is mainly localized in the epigastrium. It may also be girdling with radiation into the lum­bar region, the left shoulder blade, and sometimes the retrosternal region. Grave cases (acute necrosis of the pancreas) are manifested by excruciating pain which ends in collapse and shock. Pain is attended by nausea, painful vomiting, salivation, constipation or, less frequent­ly, diarrhoea.

Inspection of the patient reveals pallid and sometimes icteric skin and mucosa due to dif­ficult bile outflow from the common bile duct. In grave cases, general cyanosis is possible, or cyanosis may be local, on separate parts of the anterior abdominal wall or the lateral parts of the abdomen. Cyanosis is connected with pronounced toxicosis. The abdomen is often in­flated. Surface palpation of the patient with the early initial stage of the disease reveals a soft and tender abdomen; the left part is more sensitive. Later, when peritonitis joins the process, the muscles become strained and symptoms of peritoneal irritation develop. Ascites can be revealed in acute haemorrhagic pancreatitis. The pancreas is usually impalpable. Cases with skin hyperaesthesia in the upper left quadrant (corresponding to segments VII-XII) often oc­cur.

The temperature is subfebrile, high in necrotic or purulent pancreatitis, and subnormal in collapse.

The blood tests show neutrophilic leucocytosis with a shift to the left, lymphopenia, aneosinophilia, and increased ESR. During the very first hours of the disease, increased quan­tities of the pancreatic enzymes (diastase and lipase) are contained in the blood and urine. The blood and urine amylase content can nevertheless remain normal in necrotic pancreatitis (or amylase content may even be decreased). In these cases, the decreased blood calcium content and increased activity of aspartate aminotransferase are of certain diagnostic importance. At-

Special Part

Chapter 7. Digestive System

tacks of tetany can develop in marked hypocalcaemia. Hyperglycaemia and glucosuria are not infrequent.

Course. Acute pancreatitis lasts several weeks and can end by complete recovery or acute disease may convert into chronic and relapsing pancreatitis. If pancreatitis is severe, the pa­tient may die during the initial period of the disease from a collapse and shock, or later from grave complications (cysts and abscesses of the pancreas).

Treatment. The patient must be taken to hospital. The conservative therapy includes: (1) control of shock (intravenous drop infusion of 2—3 1 of a 5 per cent glucose solution, transfu­sion of blood or plasma); (2) physiological rest for the pancreas with abstention from food during 2-4 days; (3) administration of antienzymatic preparations (trasilol, etc.) for inactiva-tion of proteolytic enzymes; (4) inhibition of pancreatic secretion and removal of pains (atropine sulphate, promedol, paranephric or paravertebral block); (5) prevention of secon­dary infection (prescription of antibiotics). Surgical treatment is indicated in suppuration of the pancreas, in peritonitis, and haemorrhagic pancreonecrosis.

CHRONIC PANCREATITIS

Chronic pancreatitis occurs mostly in women aged 30 to 70. It can develop after acute pancreatitis or directly as a chronic condition due to the same aetiological factors upon which the onset of acute pancreatitis depends. Chronic pancreatitis in men occurs mostly due to chronic alcoholism.

Pathological anatomy. Morphological changes occurring in pancreatitis are oedema of the pancreas, small haemorrhages, necrosis and proliferation of connective tissue with gradual atrophy of cell elements. Reparation of the pancreas occurs simultaneously (areas of hyperplasia and formation of adenoma). Sclerosis develops in the interstitial tissues and in the parenchyma of the pancreas. Therefore the insular cells, which remain intact for a long time, are later atrophied and sclerosed. At the early stage of the disease the pancreas is only mildly enlarged and dense; cicatrices, calcification, and obstruction of the ducts develop later. The pancreas diminishes in size and becomes dense and cartilaginous.

Clinical picture. Patients with chronic pancreatitis complain of pains that come in attack or are permanent. Pain usually occurs in the upper ab­domen or in the epigastrium and radiates to the left shoulder, shoulder blade, neck, or to the left iliac bone; it can sometimes be girdling and radiate from the epigastrium, along the left costal edge, to the spine. Pain intensifies significantly after taking fatty food. The patient complains of poor appetite, aversion to fats, regurgitation, nausea, vomiting, abdominal flatulence, diarrhoea (constipation in some cases), and loss of weight. The characteristic symptom of chronic pancreatitis is ample grey and fetid fatty faeces (steatorrhoea) which is connected with developing exocrine pan­creatic insufficiency.

The skin and the sclera of the patient are sometimes icteric due to com­pression of the common bile duct by an enlarged head of the pancreas. Deep palpation of the abdomen reveals tenderness in the region of the pan-

creas. The gland can sometimes be palpated in emaciated patients as a dense band. Zones of hypersensitivity of the skin can also be revealed (Zakharyin-Head zones in the region of VIII-X segments on the left).

Neutrophilic leucocytosis and increased ESR are observed in the blood in grave cases. The content of the pancreatic enzymes in the blood and urine during exacerbation increases, but remains normal or even decreases in the atrophic process. The enzyme content in the pancreatic juice in pa­tients with severe affections of the pancreas is decreased. Hyperglycaemia and glycosuria can occur in some cases. Coprological studies show signs of inadequate digestion of proteins and fats (steatorrhoea, creatorrhoea, etc.) which is connected with pancreatic hyposecretion.

X-ray examination of the duodenum in conditions of artificial hypotonia (duodenography) reveals dilation and deformation of the duodenal loop due to enlargement of the head of the pancreas. Diagnosis is confirmed by echography.

Course. The disease is usually protracted, with periodic remissions and exacerbations. But the prognosis is usually favourable in the absence of pronounced pancreatic dysfunction or complications such as diabetes mellitus, etc.

Treatment. Bed-rest, rational and sparing diet that does not stimulate pancreatic secretion but contains sufficient amount of proteins and vitamins should be recommended during exacerbations; antibiotics and anti-enzyme preparations (trasilol and others) should also be given. Pan-creatin, pansinorm and other enzyme preparations should be given in substitution therapy.

Prophylaxis. This includes timely treatment of diseases that might be aetiologically significant in the origin of chronic pancreatitis (diseases of the bile ducts, etc.) and control of alcoholism.

31*

Chapter 8. Urinary System

Chapter 8 URINARY SYSTEM