HISTORY
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She had had a first seizure early in the morning of which she did not fully recover. On her way to our hospital, she had two more seizures lasting approximately three minutes each. During the two previous days she had been vomiting part of her food, no blood was noticed, and her drinking was increased.
There was no history of seizures in the past, not known exposure to any poison, she was not a scavenger either, nor her diet had been recently changed.
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She was dewormed (Drontal, Bayer) three days before, as she had also had some episodes of vomits afterwards. Her defecation was formed, brown stools. She was up to date with yearly vaccination, and her normal diet was dry pelleted food from a pet store (unknown brand).
CLINICAL EXAMINATION
On her arrival, she was being carried by her owner, wrapped in a blanket, and her physical examination went as follows:
l Cardiovascular system: her mucose membranes were brick red and dry, with a capillary refill time (CRT) of 1 second, a heart rate (HR) of 140 bites per minute or bpm, strong bounding femoral pulses. No heart murmur was auscultated
l Respiratory system: her respiratory rate (RR) was 20 breaths per minute (bpm), and no increased respiratory effort
l Mentation: dull, not responsive, and started having another seizure upon her initial examination
l On her abdominal palpation nothing abnormal was detected, her bladder was empty, and her owner mentioned she had been passing urine as usual. Her body condition score was 4.5/9, she had a skin tent of 2 seconds, and her rectal temperature was 38.5C. Her weight was 4.5kg.
DIFERENTIAL DIAGNOSTICS
It was made a list of the possible causes for the different symptoms presenting
Seizures and mental dullness:
Intracranial causes: neoplasia, encephalitis, trauma, vascular disease, idiopathic epilepsy
Extracranial causes: toxins, metabolic diseases, hypoglycaemia, liver disease, hypocalcaemia, uraemia, other electrolyte imbalances
Vomiting:
Gastrointestinal: dietary indiscretion, partial or total foreign body obstruction, gastroenteritis (inflammatory/infectious, parasitism, ulceration, neoplasia
Extra-gastrointestinal: pancreatitis, renal failure, hepatic disease, peritonitis, hypoadrenocorticism, drugs/toxins, central nervous system disease
Polydipsia:
Endocrine disorder: diabetes mellitus, Addisons diseas, renal disease
Septicemia: stump pyometra
Electrolyte disorders: hypokalaemia, hypercalcaemia
Shock:
Hypovolaemia: fluid loss due to vomiting, excessive urination or bleeding
SIRS secondary to toxin ingestion, hepatopathy, renal disease, gastrointestinal disease, Vera polycythemia (MM and PCV)
INITIAL STABILIZATION
In the consult room she was given 5mg of diazepam rectally (Diazepam rectal solution 5mg, Desitin), finding some fresh blood in her rectum at that moment. She was admitted immediately, placed an intravenous (IV) catheter on her right cephalic vein, and given some further 4mg of diazepam IV (0.8 ml Diazepam 10mg/2m, Roche Laboratoires) after some blood samples were drawn for investigation.
TESTS RESULTS
MINIMUM DATABASE (MDB)
Glucose: 1.3 mmol/l (2.0-8.2mmol/l)
Lactate: 6.7 mmol/l (under 2.5mmol/l)
PCV: 70% (35-55%)
TS: 6.0 g/100 ml (5.0-8.0g/l)
BUN: 15 mmol/l (2-10mmol/l)
BIOCHEMISTRY
Creatinine 189mcmol/l (20-124mcmol/l)
BUN 17.72mmol/l (1.7-7.4mmol/l)
Phosphate 3.99mmol/l (0.88-1.80mmol/l)
Total proteins 44g/l (50-72g/l)
Albumin 22g/l (26-40g/l)
Total bilirubin 35mcmol/l (0-16mcmol/l)
Total cholesterol 4.35mmol/l (2.80-8.30mmol/l)
GGT 16U/I (6-14U/I)
Glucose 1.75mmol/l (2.0-6.3mmol/l)
Calcium 0.89mmol/l (1.25-1.50mmol/l)
ACID-BASE STATUS (venous gas blood)
pH 7.36 (7.31-7.42)
PCO2 31mmHg (32-49mmHg)
HCO3 16.0mmol/l (20.0-29.0mmol/l)
Anion gap 22.6mmol/l (8-25mmol/l)
tCO2 16.9mmol/l (15-22mmol/l)
ELECTROLYTES
Sodium 142mmol/l (144-160mmol/l)
Chloride 108mmol/l (109-122mmol/l)
Potassium 4.5mmol/l (3.5-5.8mmol/l)
Na:K ratio 31.55 (over 27)
FINDINGS AND INTERPRETATION
Acid-base: a mild compensatory metabolic acidosis
Electrolytes: some mild hyponatraemia and hypochloraemia (chloride following the sodium decrease), moderate hypocalcaemia, hyperphosphataemia, and hyperbilirubinaemia
Moderate hypoalbuminaemia with hypoproteinaemia
Biochemistry: hyperglycaemia, GGT mildly elevated, moderate azotaemia
FURTHER STABILIZATION
Soon after running the MDB, her hypoglycemia was considered a live-threatening disorder, and it was addressed by giving an IV bolus of glucose 50% solution, diluted 1:1 with isotonic saline at 0.5 ml/kg. She was also given a fluid bolus of Hartmanns at 20 ml/kg over 20 minutes.
PROGRESSION
Within 30 minutes from the glucose bolus her blood glucose was checked, which had increased up to 17.5 mmol/l. On a second physical examination, her HR was 90bpm and her CRT was 2 seconds. In herself, she was bright, alert and responsive, noticing on her gait that she was a bit unstable on her feet but able to stand up and walk on her own, although with some mild proprioceptive deficits. Her pupil light reflex and menace reflex were both present and bilaterally
It was not clear if she was slightly circling to her left, due to some ataxia still present and her unwillingness to pace around.
DIAGNOSTICS DIFERENTIAL LIST
The possible causes for each of the findings went as follow:
l Erythrocytosis: heamoconcentration, true polycythaemia (Vera polycythaemia)
l Hypoglycaemia: liver failure, hypoadrenocorticism, starvation, anorexia, insulinoma, Idiopathic, bacterial septicaemia.
l Increased lactate: breathing alteration due to seizures, decreased perfusion due to her hypovolaemia
l Hypoproteinaemia: external blood loss, chronic liver failure, renal loss, gastrointestinal protein loss, malnutrition
l Azotaemia: pre-renal, renal, or post renal
l Hyperbilirubinaemia: pre-hepatic, hepatic disease
l Hyperphosphataemia: renal disease, post renal, haemolysis
l Hypocalcaemia: parathyroid disorder, secondary renal hyperparathyroidism, hypoalbiminaemia (and falsely low calcium levels)
l Elevated GGT: cholestasis, heamolysis
TREATMENT AND PROGRESSION
While she stood hospitalized she had continous fluids at 4ml/kg/h with 2.5% dextrose. She was also kept on 15mg/kg/8h cefuroxime IV (Zinacef, GlaxoSmithKline). Although she did not have any more seizures overnight, she started walking in circles to her left. During the night she passed some dark faeces (melaena) in the kennel, and was put on 0.5mg/kg/24h omeprazole orally, in addition to her treatment.
During her hospitalization period she did not pass any urine, although her bladder was palpated and roughly half full. However, an acute renal failure was of concern. By the time she was transferred to her normal practice, her blood glucose went down again to 3.2 mmol/l
CONSIDERATIONS
The appointment was at their private vet's Out Of Hours’s provider. Therefore the plan presented to her owner was focused on urgent, symptomatic treatment, aiming to transferring her back to her normal practice once she were stable for further treatment and/or investigation. Therefore, no further tests were performed, except those aimed to monitor and detect any life threatening issue, and no definitive diagnostic was reached. However, the list of issues that it was consider ruling in or out for each of the abnormalities detected, or concomitant causes was:
Ultrasound of abdominal organs: to detect any gross liver disease, renal abnormality, splenic mass as a cause for possible bleeding, cholectasis, foreign body obstruction, intussusception, or some toxicity affecting both liver and gastrointestinal tract.
ACTH test, blood cortisol levels, to assess some adrenal gland abnormality (Addison disease)
Faecal samples: to detect Giardia spp, Campilobacter spp, or Clostridium spp infection as a cause for the haemorrhagic gastroenteritis.
Culture and sensitivity test of faecal sample, which could potentially change the antibiosis plan
Intoxication: due to a sepsis, praziquantel.
In house blood smear and Diff-Quick stain
Rule out a coagulopathy disorder underneath, or Leptospirosis spp, as she had an annual vaccine with Leptospira interrogans serovar canicola and Leptospira interrogans serovaricterohaemorrhagiae (Nobivac Lepto 2, MSD Animal Health)
Other treatment to be considered: calcium supplementation to approach her hypocalcaemia, adding sucralfate to the plan if the haemorragic gastroenteritis did not improve, and continue with fluid therapy for a longer period, until her hydration were much improved.
A change in her diet, temporal or permantently.
OUTCOME
About 16h after being admitted, she was transferred to her normal practice early in the morning, when she was deemed stable to travel. Her owner did the transfer himself. Following up the case we learned she had finally being diagnosed with liver disease, and discharged a week later from her practice with a pertinent treatment and doing well.
References.
Brauer, Christina; Jambroszyk, Melanie; Tipold, Andrea. Veterinary Journal. (2011), Metabolic and toxic causes of canine seizure disorders: A retrospective study of 96 cases. Academic Journal, Vol. 187 Issue 2, p272-275.
Ablove, R.H.; Babikian, G.; Moy, O.J.; Stegemann, P.M. (2006). Elevation in compartment pressure following hypovolemic shock and fluid resuscitation: A canine model. Orthopedics, May 2006, 29(5):443-445
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