nursing

What do You Need to Know About Nursing Part in Acute Pancreatitis?

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Pancreas?

The pancreas is a small grey gland. Approximately 12-15cm in length and weighing 60-100g. It is located in the epigastric & left hypochondriac regions of the abdominal cavity.

The pancreas has roles as both an exocrine and endocrine gland. 98% of the cells within the pancreas are exocrine cells (known as acinar cells). 

  • Alpha – Glucagon’s
  • Beta – Insulin
  • Delta – Somatostatin

Normal Physiology:

Digested food is passed into the duodenum, which then stimulates the release of digestive enzymes from the duodenal epithelium. Next is the release of inactive pancreatic juices from zymogen granules (e.g., Trypsinogen). 

The digestive enzymes activate the pancreatic enzymes (e.g., Trypsinogen into Trypsin which activates phospholipid A). 

Incidence & Mortality

Acute pancreatitis 10-15%

  • Rises to 70% in patients with severely infected pancreatitis.

Severe pancreatitis – up to 30%

Mild pancreatitis – 5%

All the above should be managed in a high dependency unit – if not intensive care.

Causes of Acute Pancreatitis:

G E T S M A S H E D

  • Gall stones – 80%
  • Ethanol (alcohol) – 80%
  • Trauma
  • Scorpion Sting
  • Mumps
  • AIDS
  • Steroids
  • Hereditary hypercalcemia, hypothyroidism, hyperlipidemia 

Also, having ERCPs can stimulate/piss off the pancreas leading to acute pancreatitis.

Pathophysiology:

Inflammation from an insult or injury causes the activation of pancreatic enzymes. The enzymes cause autodigestion and fibrosis. Thrombi and necrosis of tissue cause hypocalcemia because of the fat necrosis binding to the calcium. 

Vasodilation occurs due to vessel damage. And may result in bleeding.
Phases of Damage:

  • Premature conversion of Trypsinogen to trypsin
  • Leads to apoptosis and cell death
  • Local inflammation of pancreatic tissue
  • Attracts macrophages and neutrophils, cytokines and interleukins released. Also, can be the point where it takes the form of severe pancreatitis or necrotizing. 
  • Systemic inflammation
  • SIRs
  • Organ dysfunction

Presentation:

  • Abdominal pain (localized to the epigastrium or upper abdomen) – can radiate to the back—knife, or twisting, which worsens when lying down, eating fatty foods, or consuming alcohol.
  • Vomiting 
  • Sweating
  • Pyrexia
  • Tachycardia
  • Jaundice

Delayed presentation:

  • Hypovolaemia 
  •  Abdo distension
  • Discoloration of the lumbar region (Grey Turner’s sign)
  • Peri-umbilical discoloration (Cullens sign)
  • Organ dysfunction

Blood tests:

  • Amylase is pancreatitis specific, as is lipase.
  • CRP, ALT increase
  • Also, depending on the severity, you may see:
  • low calcium
  • increased WBC
  • increased BUN
  • Low Hct
  • High glucose

Diagnosis tools:

  • Ransom’s Criteria
  • Modified Glasgow criteria

Cardiovascular complications and treatment:

  • Hypovolemia
  • Fluid replacement
  • Consider ITBV/CO/CVP
  • Vasopressors to increase SVR

Respiratory complications:

  • Gross ascites
  • Atelectasis
  • Hyperventilation (pain)
  • Pleural effusion
  • ARDS
  • Noncardiogenic pulmonary edema (occurs in 10-30% of cases)
  • Pseudocyst or abscesses in the chest cavity
  • Up to 70% of patients have hypoxemia 

Coagulation abnormalities:

  • Trypsin activates prothrombin and plasminogen
  • DIC
  • Pulmonary emboli
  • Intravascular thrombi
  • Hemorrhage into GI tract or peritoneal cavity
  • Hemorrhagic pseudocyst – arterial embolization

Electrolyte imbalances/renal:

  • Hypokalemia
  • Hypocalcemia
  • Blood glucose 
  • Amylase and lipids should be monitored also
  • Hypovolemia & hypotension
  • Clots may form in the renal artery or vein
  • Monitor urea/creatinine
  • Appropriate renal support (filter) 

Pain & Analgesia

  • IV morphine is the drug of choice
  • Longer half-life
  • increased spasm of the sphincter of Oddi
  • Pethidine
  • Epidural/nerve blocks
  • PCA
  • Positioning/relaxation

Nutrition – TPN vs. Enteral

TPN for people who are NBM – it is expensive, causes metabolic alterations, and has a much higher risk of infection in comparison to enteral.

Enteral feeding is shown to be as good as TPN. It reduces the need for surgical intervention and reduces hospital stay, but a further comparison of Parenteral and Enteral feeding shows no difference in mortality rate.

Infection:

  • 80% of fatal acute pancreatitis is due to septic complications
  • BSG guidelines – antibiotic should not be given > 14 days in the absence of +ve culture
  • Research revealed no added benefit to giving prophylactic antibiotics

Intra-Abdominal Pressure:

Normally <5. It can be 15> in AP, which can alter splenic perfusion and decrease renal perfusion. Reduced CO and increased SVR as well as increased airway pressures.

Surgical intervention may be needed for decompression.

If IAP >20-30, abdominal compartment syndrome can occur.

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In the course of their work, a consultant may be involved in any of the following:

  • Maintain the confidentiality of your practice
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  • Identify standards of care, causation, and damage issues
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  • Prepare chronologies of medical events and compare and correlate them to allegations
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