Clinical Notes: Brachen

Brachen was involved in a road traffic accident 36 hours prior to presentation. Now he is nearly collapsed, depressed and vomiting.

   Brachen
 

Learning Objectives

  1. Identification of life-threatening abnormalities in a collapsed patient.
  2. Arriving at an accurate diagnosis, formulating a treatment plan and dealing with complications.
  3. Determining if azotemia is pre-renal, renal or post renal.
  4. Understanding the aetiology and management of post-renal azotemia.

Clinical Condition

Azotemia occurs when the normal system of nitrogenous waste removal by the kidneys is disrupted. This can occur acutely or chronically and may be classified, by the site at which the insult occurs leading to the azotemia, into pre-renal, renal or post-renal.

Inadequate blood flow to the kidneys such as occurs during hypovolemic shock or cardiac failure can cause a pre-renal azotemia. Toxic insults to the kidney, such as ethylene glycol poisoning or infections (e.g. Leptospiro) can result in azotemia due to failure of the normal function of the nephrons. Obstruction or rupture of the urinary tract distal to the renal pelvis will result in a post-renal azotemia.

Azotemia is a laboratory diagnosis and only describes a biochemical change. Uremia is the term used to describe azotemia and the associated clinical signs (e.g. vomiting, halitosis, pu/pd, anorexia, vomiting, lethargy).

In Brachen's case the ruptured bladder allowed the urine formed by the kidneys to flow into the peritoneum. Due to the concentrating actions of the kidney urine has a much higher concentration of waste metabolites such as urea, creatinine and potassium than blood. These will then diffuse back into the blood from the peritoneal space. Smaller molecules such as urea will equilibrate most rapidly.

The presence of urine in the abdominal cavity will produce a marked inflammatory response. Inflammatory cells, and protein rich fluid will pour into the abdomen. Reduced fluid intake and increased losses by vomiting and fluid accumulation in the peritoneal cavity result in hypovolemia and dehydration. Compensatory tachycardia may be seen, but hyperkalemia can cause bradycardia, if sufficiently severe. Poor pulse quality and tacky mucus membranes are often detected.

This build up of potassium and urea in the blood as well as loss of circulating volume leads to the classical (but fairly non specific) signs of acute renal failure: vomiting, weakness and anorexia as well as cardiovascular collapse.

Depending on the nature of the damage to the urinary tract some patients present with a history of dysuria, but some may still be urinating. Abdominal enlargement and a fluid thrill are often detected during physical examination.

Case Management

Important points in management of collapsed patients

  1. Rapid assessment of the patient to identify which body system(s) are primarily involved.
  2. Obtaining intravenous access.
  3. Obtaining appropriate laboratory samples before initiating treatment.

Management of cardiovascular collapse

  1. Correct identification of cause of cardiovascular collapse.
  2. Identify and characterise any dysrythmias present.
  3. Rapid infusion of appropriate fluids or pharmacological intervention to promote cardiac output.
  4. Plan a definitive treatment plan for the underlying condition.

Management of uroabdomen

  1. Shock rate fluid administration to restore circulating volume
    • Polyionic isotonic crystalloid solutions incorporating a source of bicarbonate to reduce metabolic acidosis are preferred.
    • Colloids may be indicated especially if the protein levels are low or low relative to the degree of dehydration.
  2. Drainage of abdomen
    • Drainage of urine from the abdomen prior to investigation of the cause of the condition may be required to improve patient ventilation, comfort or to remove the source waste that is being resorbed into the circulation.
    • This should be undertaken slowly and with care as sudden release of the fluid can precipitate massive cardiovascular collapse and death. Start fluid therapy first.
    • A peritoneal lavage catheter will make the process easier as it has multiple openings, which are less easily blocked by omentum. Local anaesthetics should be used.
    • Placement of an indwelling urinary catheter may assist in preventing additional urine leaking from a ruptured bladder.
  3. Identification of the damage to the urinary tract.
    • Sites of damage to the urinary tract can include avulsion of the ureter from the renal pelvis or bladder, bladder rupture or urethral rupture.
    • Ultrasound examination of the bladder is often sufficient to diagnose a ruptured bladder.
    • Contrast radiography or fluoroscopy may be required to confirm ureteral or urethral damage. Intravenous urethrography, contrast cystography or retrograde urethrography may be used.

Stabilisation of patient prior to anaesthesia and surgery

  1. Correcting hyperkalemia and reducing axotemia and acidosis.
    • This is necessary to optimise patient safety under anaesthesia. Acidosis and azotemia will affect the patient's response to anaesthetic drugs and may promote dysrythmias.
    • Fluid therapy combined when necessary with abdominal drainage is the mainstay of achieving these aims. Hartmann's solution is as close to ideal as is currently available on the commercial market. It is polyionic and contains a source of bicarbonate (lactate). There is a small amount of potassium in the solution, but as its concentration is lower than that in a hyperkalemic patient it will, by dilution, lower the patients serum potassium concentration.
  2. Selection of anaesthetic agents
    • Sedation may be required to complete imaging or abdominocentesis/drainage. Agents chosen should have minimal effects on the cardiovascular system. Analgesia, sufficient for surgery, must be given consideration. A synergistic mixture of an opioid and a sedative will normally give better results, with fewer side effects, that a larger dose of a single agent.
    • Induction and maintenance agents also should have minimal cardiovascular effects. Normalising electrolyte and acid base disturbances, and correcting azotemia prior to induction of anaesthesia, will greatly enhance safety regardless of the agents chosen. However, this is not always possible.
    • Azotemic patients often respond unpredictably to anaesthetic agents. Whatever agent is used should be given very slowly and to effect.
    • Azotemic patients often vomit and mask induction may increase the risk of aspiration of vomitus during induction.
    • A familiar technique in a well stabilised patient is generally safer than something theoretically safer but unfamiliar. Equally, theoretically safer drugs are no substitute for patient preparation and stabilisation.
  3. Postoperative care of the patient
    • Postoperative fluid therapy must be maintained at a rate sufficient to correct any remaining dehydration and match ongoing losses and maintaince requirements
    • Analgesia
    • Antibiotics

Suggested Management Plan for Brachen

  1. ABC - A rapid assessment of Brachen reveals a marked tachycardia and poor pulses. Respiratory function appears normal.
  2. There is no immediately life-threatening abnormality so a full physical examination can be performed. This confirms cardiovascular collapse and highlights a painful fluid-filled abdomen.
  3. A catheter should be placed to secure venous access, even if fluids are not administered immediately. As the patient deteriorates it will become progressively more difficult to place an intravenous catheter.
  4. A number of procedures could be carried out next. Blood samples can be collected for laboratory analysis or imaging undertaken to further characterise the abdominal problems. Samples of the abdominal fluid should be taken and submitted for appropriate laboratory analysis.
  5. Once blood samples are collected intravenous fluid therapy can start. In practice with such collapsed patients the initial choice of fluid given may have to be made without the benefit of laboratory results.
  6. Once a diagnosis has been reached and appropriate fluid therapy initiated, anaesthesia should be induced and an exploratory laparotomy performed. The abdomen can then be drained, lavaged and the damaged bladder repaired. In selecting the drugs to be used for the anaesthetic protocol consideration has to be given to selecting agents for premedication that have minimal effects on the cardiovascular system (diazepam/midazolam) and provision of sufficient analgesia for abdominal surgery (pethidine, methadone, morphine).
  7. Postoperative analgesia should be given.

These tasks have to be performed to complete the case simulation. Additional tasks that may be considered on a case-by-case basis would include the provision of appropriate antibiotics, placement of an indwelling urinary catheter, anti-emetics, diuretics to counteract acute renal failure and management of concurrent injuries.

Further Reading

  1. RVC Clinical Notes - Renal and Anaesthesia sections
  2. Small Animal Surgery (2nd Ed) Edited by Fossum
  3. BSAVA Emergency and Critical Care Manual. Edited by King and Hammond

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