Peritonitis, haemoabdomen & uroabdomen Flashcards
Types of peritonitis
- septic
- aseptic
Causes of septic peritonitis & their CS/Hx
Intestinal perforation
- FB ingestion
- scavenger
- v+
- pain
Haematogenous
- distributive shock
External - penetrating
- usually obvious
Iatrogenic
- e.g. recent sx
- pain
- distributive shock
- v+
Urinary ascension
- reduced volume/increased frequency
- stranguria/dysuria
- pain
- haematuria
Causes of aseptic peritonitis & their CS/Hx
Pancreatitis - enzyme leakage
- acute abdomen (pain)
- v+
- PUPD
- organ specific signs
Hepatitis
- acute abdomen (pain)
- v+
- PUPD
- organ specific signs
Cholangitis
- acute abdomen (pain)
- v+
- PUPD
- organ specific signs
Splenitis
- acute abdomen (pain)
- v+
- PUPD
- organ specific signs
Nephritis
- acute abdomen (pain)
- v+
- PUPD
- organ specific signs
Neoplasia
- pain
- weight loss
- age: usually older
- specific signs dependent on location
Bile
- acute abdomen: pain
- jaundice
- v+
Urine
Blood
Gastric perforation
- abdo pain: rupture -> reduced pain
- v+
- anorexia
- hx of scavenging/chronic v+
Peritonitis - diagnostics
POCUS
- any pt with abdominal discomfort should have POCUS performed
Free fluid?
- tap it
Physical appearance of the fluid
- septic or aseptic?
Glucose measurement on the fluid
- 1mmol/l less than blood supportive of septic fluid
Lactate measurement on the fluid
- 2mmol/l more than blood supportive of septic fluid
Cytology
- intracellular bacteria, but this does take time and takes you away from the pt
Diagnostic peritoneal lavage
- instill 22ml/kg warmed saline into the abdomen via a large bore catheter, then retrieve a sample (lactate and glucose less useful with this)
- always do a C&ST
Peritonitis - tx
Source control is key
Depends on the source:
- surgical removal if it can be excised (e.g. perforated intestine)
- abdominal drain ± lavage if the source is non-removable
Stabilise the pt 1st e.g. treat the distributive shock and the associated complications such as arrhythmias
Antibiotics if septic - escalate vs de-escalate
Escalate - start with no antibiotics (or a single antibiotic e.g. amoxy-clav) and wait for C&ST results or pt deterioration before adding others in
De-escalate - start with double or triple combination antibiotics (e.g. amoxy-clav, metronidazole and marbofloxacin) and then reduce depending on C&ST results
Haemoabdomen - diagnostics
Clinical signs
- hypovolaemia
POCUS
Tap free fluid
- PCV on fluid
Blood PCV vs fluid PCV
- PCV same: haemoabdomen, acute
- PCV of fluid is higher: semi acute bleed (some compensation of volume has occurred)
- PCV of fluid is lower: chronic bleed, e.g. cancer
Haemoabdomen - monitoring & tx
Monitoring
- for hypovolaemic shock
Loss of RBCs
= loss of O2 carrying capacity -> cerebral hypoxia (dull mentation)
Transfusion dependant or not?
Blood pressure
- MAP >60mmHg (minimum, ideal >70)
Lactate
- <2.0mmol/l
Baseline parameters then fluid bolus (10ml/kg, isotonic crystalloid and reassess
Next steps depends on cause
Causes of haemoabdomen
- neoplastic bleeds
- trauma
- coagulopathy
Neoplastic bleeds tx
If response to fluid bolus is poor -> transfusion
- auto-transfusion vs whole blood vs pRBC + plasma
Definitive tx:
- surgery ± chemo/radiotherapy
- euthanasia
Types of trauma
- blunt e.g. RTA
- penetrating e.g. stick/knife
Blunt trauma tx
If response to fluid bolus is poor -> transfusion
- autotransfusion vs whole blood vs pRBC + plasma
Definitive tx:
- wait
Conservative tx:
- tranexamic acid (anti-fibrinolytic, maintains clot stability)
- repeat transfusions
Probably not bleeding from a single location
- multiple locations likely all with a small volume
- don’t recommend ex-lap
If still bleeding after 3rd transfusion and tranexamic acid
- consider surgery
- consider abdo wrap: create pressure wave across the entire animal
Penetrating trauma tx
If response to fluid bolus is poor -> transfusion
- autotransfusion vs whole blood vs pRBC + plasma
– consider plasma as losing clotting factors
Definitive tx:
- operate: stabilise and cut, don’t wait
– need to get in and find problem quickly
- consider a staged approach: pack it & close & come back a day later
- tranexamic acid (anti-fibrinolytic, maintains clot stability)
Coagulopathy tx
If response to fluid bolus is poor -> transfusion
- autotransfusion vs whole blood vs pRBC + plasma
Definitive tx
- depends on cause
- clotting factors: fresh frozen plasma (FFP)
- thrombocytopenia: platelet rich plasma (PRP)
- rat poison: vitamin K (+ FFP)
- treat the underling dz
Uroabdomen - history
- urinary signs (stranguria/dysuria)
- previous surgery (cystotomy)
- trauma (RTA)
Uroabdomen - CS
- abdo pain
- reduced mentation
- inappropriately low HR (due to hyperkalaemia)
Uroabdomen - diagnosis
History
CS
POCUS
- free fluid -> tap it
Radiography
ECG
- cardiogenic shock
Free fluid analysis to confirm uroabdomen:
- creatinine >2x blood value
- potassium >1.4x blood (dogs), >1.9 blood (cats)
Hyperkalaemia can be life threatening
- >8.0mmol/l -> risk of atrial standstill
Hyperkalamia - what to do?
Protect the cardiac action potential
- calcium gluconate: slow IV (can cause arrhythmia itself) (aim to give as bolus over 30mins) (stabilises the cardiac action potential)
Source control:
- urinary catheter (buys time as the urine drains via the catheter preferentially, and you can consider delayed surgery or referral)
- abdominal lavage
- surgery to repair leakage
Hyperkalaemia - physiological manipulation
Acidaemia promotes hyperkalaemia
- Hartmann’s is alkalinising
- give Hartmann’s
- do NOT give saline as is acidifying and will make this worse
Bicarbonate
- adjunct
- manipulates sodium movement: sodium load the cell, stimulates potassium uptake from the blood
Glucose/insulin effect
- glucose bolus: glucose gets rid of potassium by stimulating insulin release
- if glucose bolus fails give insulin
- insulin: if give insulin need to supplement glucose as otherwise will become hypoglycaemic
- if insulin fails go for bicarb
- beta agonist e.g. salbutamol stimulate the Na/K pump, pushing potassium into cells in exchange for sodium, last resort
