Chauke NJ 201908564 NUTRITIONAL SCREENING

UNIVERSITY OF LIMPOPO
FACULTY OF HEALTH SCIENCES
SCHOOL OF HEALTH CARE SCIENCES
DEPARTMENT OF HUMAN NUTRITION AND DIETETICS
Surname & Initial(s) : CHAUKE NJ

Student Number : 201908564
Module : Diet Related Disoders
Module Code : MDIB031
Submission Date : 07 February 2022
Facilitator (s) : Mr Ndhambi
NUTRITIONAL SITUATION IN SOUTH AFRICANS
Table of content
1|Page
Introduction 2
Pathophysiology of acute pancreatitis 2
Signs and symptoms 2&3
Complications of acute pancreatitis 4
Management of acute pancreatitis 5
References………………………………………………………………………………………………7
2|Page
Introduction
Acute pancreatitis
(Cox, Conlon, 2020 ) reported that Acute pancreatitis affects 300 to 600 new patients
per million population per year and is most caused by gallstones or alcohol. Diagnosis is
made by a combination of a typical presentation (upper abdominal pain and vomiting) in
conjunction with raised serum amylase (more than three times the upper limit of normal)
and/or lipase (more than twice the upper limit of normal). Several other acute abdominal
emergencies can mimic acute pancreatitis and may be associated with a raised serum
amylase. This assignment talks about the pathophysiology, signs and symptoms,
complications, and management of Acute pancreatitis
Pathophysiology of acute pancreatitis
pancreatitis develops because of an injury or disruption of the pancreatic acinar, which

permit the leakage of pancreatic enzymes (trypsin, chymotrypsin, and elastase) into
pancreatic tissue. The leaked enzymes become activated in the tissue, initiating
autodigestion and acute pancreatitis. The activated proteases (trypsin and elastase)
and lipase break down tissue and cell membranes, causing edema, vascular damage,
hemorrhage and necrosis.
The initial phase is characterized by intrapancreatic digestive enzyme activation and

acinar cell injury. Trypsin activation appears to be mediated by lysosomal hydrolases
such as cathepsin B that become colocalized with digestive enzymes in intracellular
organelles. The second phase of pancreatitis involves the activation, chemoattraction,
and removing of leukocytes and macrophages in the pancreas, resulting in an
enhanced intrapancreatic inflammatory reaction. The third phase of pancreatitis is
because of activated proteolytic enzymes and cytokines, released by the inflamed
pancreas, on distant organs. Activated proteolytic enzymes, such as trypsin, not only
digest pancreatic tissues but also activate other enzymes such as elastase and
phospholipase A2. The active enzymes and cytokines then digest cellular membranes
and cause proteolysis, edema, interstitial hemorrhage, vascular damage, coagulation
necrosis, fat necrosis, and parenchymal cell necrosis.
Signs and symptoms of acute pancreatitis
3|Page
 Acute epigastric and peri-umbilical pain - abdominal pain is the major symptom of
acute pancreatitis. Pain may vary from a mild discomfort to severe, constant, and
incapacitating distress. the pain, which is steady and boring in character, is in the
epigastrium and periumbilical region, and may radiate to the back, chest, flanks,
and lower abdomen.
 Nausea and vomiting
 increased formation and release of kinin peptides, which cause vasodilation and
increased vascular permeability
 Abdominal distension associated with a small bowel ileus
 pseudocyst in severe disease
 Low grade pyrexia, occasionally hypothermia
 Shock (increased pulse rate, decreased blood pressure)
 Retroperitoneal haemorrhage showing as either Grey Turners sign–grey
discolouration (bruising) over the flanks
 Cullen’s sign–bruising in and around the umbilicus. (Adam and Osborne, 2005)
Complications of acute pancreatitis
 Acute peripancreatic fluid collection -peripancreatic fluid associated with

interstitial oedematous pancreatitis with no associated peripancreatic necrosis
 Walled-off necrosis - a mature, encapsulated collection of pancreatic or extra
pancreatic necrosis that has developed a well-defined inflammatory wall
 Necrotizing pancreatitis- Inflammation associated with pancreatic parenchymal
necrosis and/or peripancreatic necrosis
 Interstitial pancreatitis -Acute inflammation of the pancreatic parenchyma and
peripancreatic tissues, but without recognizable tissue necrosis
 Splenic and portal vein thrombosis-The use of CT to monitor progress has

resulted in the increased recognition of splenic and segmental portal vein
thrombosis. Splenic vein thrombosis does not usually require treatment, but
thrombus in the portal or superior mesenteric vein requires anticoagulation either
with low molecular weight heparin
4|Page
 Gastrointestinal Haemorrhage Poorly controlled sepsis within a collection can
present with acute internal haemorrhage into a collection, or bleeding from a
drain site.
 Metabolic complications include hyperglycemia, hypertriglyceridemia.

 Pancreatic pseudocyst - An encapsulated collection of fluid with a well-defined
inflammatory wall usually outside the pancreas with minimal or no necrosis. This
entity usually occurs >4 weeks
 Pancreatic ascites-This condition rarely occurs in association with acute
pancreatitis, but when it does it is due to spontaneous decompression of a
pancreatic pseudocyst, with escape of pancreatic juice into the peritoneal cavity.
Amylase-rich fistula fluid is common after percutaneous drainage, when internal
control can often be successfully achieved by endoscopic transpupillary
drainage.
 Cardiovascular complications include hypotension, hypovolemia, nonspecific
ST-T changes in electrocardiogram simulating myocardial infarction and
pericardial effusion
Management and treatment
Antibiotics The dual peak in mortality in acute pancreatitis is well recognized. The late
peak is determined by complications associated with necrosis, including the
development of pancreatic or peripancreatic infection. The consensus of the most
recent systemic reviews is that there is no evidence supporting the use of prophylactic
antibiotics in either mild or severe acute pancreatitis, and the recommendation is to
avoid their use, using targeted antibiotic therapy for episodes of proven infection. It is,
however, reasonable to commence antibiotics in the deteriorating patient with
radiological and clinical evidence of sepsis while awaiting culture confirmation. (Chris,
Gardner, 2015)
5|Page
Nutrition support- assisted feeding may be required in severe acute pancreatitis to
provide long-term nutritional support. Randomized studies have shown that enteral
nutritional support is cheaper and is associated with fewer side effects than total
parenteral nutrition. It has been suggested that nutritional support may help to preserve
mucosal function and limit the stimulus to the inflammatory response. People with
severe acute pancreatitis are admitted to intensive care unit, where vital signs (pulse,
blood pressure, and rate of breathing) and urine production can be monitored
continuously. They are given nutrition via tube feeding. If tube feeding is not possible,
people are given nutrition through an intravenous catheter that has been inserted into a
large vein; that is intravenous feeding.
Fluid Resuscitation and Monitoring Response to Therapy - probable pulmonary

oedema and diaphragmatic splinting. Monitor respiratory rate, arterial blood gases and
blood-oxygen saturation. The most important treatment intervention for acute
pancreatitis is safe, aggressive intravenous fluid resuscitation. The patient is made NPO
to rest the pancreas and is given intravenous narcotic analgesics to control abdominal
pain and supplemental oxygen (2 L) via nasal cannula.
Follow-Up Care - hospitalizations for moderately severe and severe acute pancreatitis
can be prolonged and last weeks to months and often involve a period of intensive care
unit admission and outpatient rehabilitation or subacute nursing care.
6|Page
References
Adam S, Osborne S .Critical Care Nursing: Science and Practice. 2nd edition. Oxford
University Press,
Chris E. Forsmark Timothy B. Gardner: Prediction and Management of Severe Acute

Pancreatitis. New York Pg, 2015 pg 110-114
J. Larry Jameson et al. Harrisons Principles of Internal Medicine: Acute pancreatitis:

20th Edition (Vol.1 Vol.2).15/26
J Firth ,T Cox, Conlon C: Oxford Textbook of Medicine: gastrointestinal Disorders;

Acute pancreatitis,3209 .Oxford, 2020
7|Page

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UNIVERSITY OF LIMPOPO

FACULTY OF HEALTH SCIENCES

SCHOOL OF HEALTH CARE SCIENCES

DEPARTMENT OF HUMAN NUTRITION AND DIETETICS

Surname & Initial(s) : CHAUKE NJ

NUTRITIONAL SITUATION IN SOUTH AFRICANS

Pathophysiology of acute pancreatitis

pancreatitis develops because of an injury or disruption of the pancreatic acinar, which

The initial phase is characterized by intrapancreatic digestive enzyme activation and

Signs and symptoms of acute pancreatitis

Complications of acute pancreatitis

 Acute peripancreatic fluid collection -peripancreatic fluid associated with

 Splenic and portal vein thrombosis-The use of CT to monitor progress has

 Metabolic complications include hyperglycemia, hypertriglyceridemia.

Management and treatment

Fluid Resuscitation and Monitoring Response to Therapy - probable pulmonary

Chris E. Forsmark Timothy B. Gardner: Prediction and Management of Severe Acute

J. Larry Jameson et al. Harrisons Principles of Internal Medicine: Acute pancreatitis:

J Firth ,T Cox, Conlon C: Oxford Textbook of Medicine: gastrointestinal Disorders;

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