ICU & Referral Case Log

30Days on rotation
7Specialties
12Cases logged
4Protocols
Student notes from a 30-day clinical rotation, written for my own revision. Signalment and case details are generalised, and no patient, client or clinician is identifiable. Not clinical guidance, and not for use in treatment decisions.

Thirty days at a specialty referral centre is a different world from general practice or university rotations. You don't see healthy animals coming in for vaccinations. Everything that walks through the door is already complicated — chronic, referral, or emergency. You adapt fast or you fall behind.

These are my notes. Some are full write-ups, some are lines I scribbled between cases. The index below is the fastest way in.

Case index

Filter
#Presentation / diagnosisSignalmentSystem
01 Protein-losing enteropathy with lymphangiectasia Canine · geriatric F entire · <2 kg GI
02 PLE + PLN with hypocalcaemic seizures Canine · middle-aged MN · ~3 kg GI · Renal
03 Idiopathic lymphoplasmacytic rhinitis Canine Respiratory
04 Regenerative anaemia + gallop — suspected haemoplasma / HCM Feline · young adult MN Cardio · Haem
05 Tenesmus and diarrhoea with thrombocytopenia Canine · senior small breed GI
06 Suspected Evans syndrome (IMTP + IMHA) Feline · senior Immune · Haem
07 Cluster seizure episodes — metabolic workup Feline · juvenile Neuro
08 Hindlimb hypermetric "horse-walk" gait Canine · small breed Neuro
09 Acute vomiting and recumbency after sea water Canine · young adult entire Toxicology
10 Icterus with fever — suspected leptospirosis Canine Hepatic · Infectious
11 Common viper envenomation Canine Toxicology
12 Pelvic fracture, hit by car Canine Trauma · Ortho

12 cases

1 · Cases

Cases I followed closely enough to write up properly.

01 — Protein-losing enteropathy with lymphangiectasia

Signalment
Canine, geriatric, female entire, toy-breed terrier, <2 kg
Presentation
Chronic diarrhoea, anorexia and progressive weakness over several weeks, with repeated visits to the clinic. Markedly underweight and exhausted on presentation.
Key findings
Hypoalbuminaemia (albumin 1.2–2.2 g/dL), anaemia (PCV as low as 16%), intermittent hypoglycaemia. Free fluid in abdomen and thorax. Thickened intestinal loops.
Diagnosis
PLE secondary to chronic inflammatory enteropathy with lymphangiectasia, confirmed on endoscopic biopsy (lymphangiectasia with crypt abscesses). Concurrent pancreatitis; small cell lymphoma on the differential list.
Outcome
Stabilised and discharged on medical management. Prognosis guarded.

Treatment:

  • Prednisolone ½ tablet (5 mg) SID — anti-inflammatory / immunosuppression
  • Co-amoxiclav and metronidazole — pending biopsy results
  • Omeprazole — gastric protection
  • Maropitant — nausea
  • Ursodeoxycholic acid — bile flow support
  • Mirtazapine, transdermal — appetite stimulation. Applied to the pinna, which is a genuinely useful route in a patient this size that will not take tablets
  • Cobalamin injections — weekly
  • Vitamin K — during hospitalisation, for coagulation support

Diet: ultra low-fat gastrointestinal diet plus hypoallergenic options. Low fat is the cornerstone with lymphangiectasia — dietary fat drives lymphatic distension and protein loss.

Complications to watch for:

  • Thromboembolism — hypoproteinaemia plus inflammation is a pro-thrombotic state
  • Urinary tract infection and pyometra — entire and immunosuppressed is a bad combination
  • The feeding tube was dislodged during hospitalisation and had to be replaced

What I actually learned: how much of this case was owner communication. The prognosis is guarded and the treatment is long and expensive. Being honest about that while keeping an owner motivated to continue is harder than any of the medicine.

Low-fat diet · cobalamin · immunosuppression — the three pillars in PLE with lymphangiectasia.

02 — PLE and PLN with hypocalcaemic seizures

Signalment
Canine, middle-aged, male neutered, small breed, ~3 kg
Presentation
Seizures, chronic intermittent diarrhoea, progressive weight loss.
Key findings
Marked hypoproteinaemia and hypoalbuminaemia, hypocalcaemia, hypokalaemia, hypophosphataemia, leukocytosis with neutrophilia, thrombocytopenia. UPC > 2. cPLI raised initially, but imaging did not support active pancreatitis.
Diagnosis
Protein loss from both ends — PLE (suspected lymphangiectasia with IBD) alongside PLN. Seizures attributed to electrolyte derangement, principally hypocalcaemia, rather than primary epilepsy. PARR excluded lymphoma.
Outcome
Stabilised on immunosuppression with a tapering plan. Seizures resolved once the electrolytes were corrected.

Medications:

  • Cyclosporine 0.15 ml BID (later tapered)
  • Prednisone — tapered from daily to every other day
  • Spironolactone — later discontinued
  • Rivaroxaban — anticoagulation for the thromboembolic risk that comes with PLE
  • Omeprazole
  • Mirtazapine PRN
  • Cobalamin and folate — oral and injectable
  • Doxycycline — discontinued after a negative vector-borne panel

Procedures: plasma transfusion, IV fluids with electrolyte correction, levetiracetam for seizure control, endoscopy with gastrointestinal biopsies under general anaesthesia, and PARR testing.

Note on ciclosporin: a calcineurin inhibitor that blocks T-cell activation. Side effects worth knowing: gastrointestinal upset, gingival hyperplasia, hepatotoxicity, nephrotoxicity and hypertrichosis. A workhorse drug in immune-mediated disease.

Seizures in a hypoalbuminaemic dog — check calcium before you reach for epilepsy.

03 — Idiopathic lymphoplasmacytic rhinitis

Signalment
Canine
Presentation
Continuous nasal discharge with reverse sneezing.
Diagnosis
Diagnosis of exclusion. Fungal, bacterial and neoplastic causes ruled out; biopsy showed lymphoplasmacytic inflammation.
Outcome
Medical management. A frustrating condition, because there is no confirmatory test.
Where there is no confirmatory test, the workup is the diagnosis. Document what you excluded, and why.

04 — Regenerative anaemia with a gallop rhythm

Signalment
Feline, young adult, male castrated, purebred
Presentation
Weakness, anorexia for several days, dehydration, significant weight loss and pica. Antibiotics had been stopped a couple of days before presentation.
Key findings
Pale mucous membranes, gallop heart sound, enlarged stomach and intestines on imaging. New methylene blue stain consistent with a regenerative anaemia. Urea 122, phosphorus 8.9, total protein 10, globulins 6.3, ALT 104, with decreased chloride and bicarbonate.
Working diagnosis
Regenerative anaemia, suspected haemoplasmosis (Mycoplasma haemofelis), with azotaemia of renal or pre-renal origin. Hypertrophic cardiomyopathy considered given the gallop.
Outcome
Still under investigation when I finished the rotation.
A gallop in an anaemic cat is not automatically cardiac — but it does mean the heart needs looking at before you volume-load.

05 — Tenesmus and diarrhoea with thrombocytopenia

Signalment
Canine, senior, small breed
Presentation
Diarrhoea, tenesmus, dehydration.
Key findings
Thrombocytopenia, with gastroenteritis on the differential list.
Differentials
Vector-borne disease, severe gastroenteritis, or neoplasia — transitional cell carcinoma or prostatic carcinoma given the tenesmus.
Tenesmus in a senior dog is a urogenital sign until proven otherwise. Don't let "diarrhoea" anchor you.

06 — Suspected Evans syndrome

Signalment
Feline, senior
Presentation
Vomiting and diarrhoea, anorexia, dehydration.
Key findings
Thrombocytopenia and neutropenia. Ultrasound showed a solitary kidney, ascites, ileus, and an enlarged lumbosacral lymph node.
Working diagnosis
Evans syndrome — concurrent immune-mediated thrombocytopenia and immune-mediated haemolytic anaemia.

07 — Cluster seizure episodes in a juvenile cat

Signalment
Feline, a few months old
Presentation
Episodes of roughly 45 seconds to a minute — hypersalivation, disorientation, running, and seizure activity. The owner described the cat as "drunk" between episodes.
Differentials
Congenital portosystemic shunt, infectious causes, or metabolic derangement including diabetic ketoacidosis.
Management
Diazepam for acute control while the metabolic workup ran.
Seizures in a young cat that stays disorientated between episodes — a shunt belongs near the top of the list, not the bottom.

08 — Hindlimb hypermetric "horse-walk" gait

Signalment
Canine, small breed
Presentation
Exaggerated, high-stepping hindlimb gait.
Interpretation
A proprioceptive deficit or a specific spinal or neuromuscular lesion — localise before building the differential list.
Treatment
Metamizole (analgesia and antipyresis), pregabalin (neuropathic pain), diazepam (muscle relaxation).

09 — Acute vomiting and recumbency after sea water

Signalment
Canine, young adult, entire. Fed a dry kibble diet.
Presentation
Taken to the sea in the morning, began vomiting, and within an hour was unable to stand. No vomiting at home beforehand.
Differentials
Salt-water toxicosis with hypernatraemia, severe gastroenteritis, or an acute abdomen.
Correct hypernatraemia slowly. Dropping sodium too fast is how a salvageable case turns into cerebral oedema.

10 — Icterus with fever, suspected leptospirosis

Signalment
Canine
Presentation
Possible toxin exposure. Icteric mucous membranes on examination, pyrexia (38.7 °C), general condition otherwise fair.
Working diagnosis
Suspected leptospirosis. A zoonosis, so barrier nursing and staff precautions from the moment it appears on the list.
Treatment
Hospitalisation with isotonic crystalloids, plus hepatoprotective support: SAMe 20 mg/kg SID, N-acetylcysteine 140 mg/kg then 70 mg/kg, vitamin E, omega-3 fatty acids and coenzyme Q10.
Once leptospirosis is on the differential list it changes how everyone in the building handles the patient, not just the treatment plan.

12 — Pelvic fracture, hit by car

Signalment
Canine
Presentation
Road traffic accident with pelvic fracture.
Management
Pelvic fractures are frequently managed conservatively. The decision points are neurological deficits, inability to urinate, and collapse of the pelvic canal.
In a road traffic case, the fracture is the obvious injury and rarely the one that kills. Thorax, bladder and perfusion first.

2 · Protocols

Presentations common enough here that I wrote out the whole approach.

Common viper envenomation (Vipera palaestinae, "tzefa")

The common viper is the main culprit in Israel. Bites cluster in summer, usually to the face or limbs, and owners frequently do not witness the bite — they notice sudden swelling. A common presentation in a referral emergency setting.

What you'll see: rapid and often dramatic local oedema, tachycardia, tachypnoea, lethargy and drooling. The dangerous part is the coagulopathy — check PT and aPTT early, because DIC can develop fast.

Approach:

  • Stabilise first — IV access and crystalloids for hypotension and shock. Keep the animal calm and minimise movement; movement spreads venom
  • Monitor — minimum 24 hours hospitalisation. CBC, biochemistry, coagulation panel, blood pressure and ECG, repeated every few hours
  • Analgesia — these bites hurt
  • Antihistamines — used in some protocols, evidence limited
  • Antibiotics — controversial; used in some protocols for secondary infection risk
  • Antivenom — the only specific treatment. Indicated for shock, severe or rapidly progressing oedema, coagulopathy or haemorrhage. The dose is titrated to effect, not fixed. Infuse slowly, watch for anaphylaxis, and have adrenaline drawn up
Corticosteroids are contraindicated — retrospective work links steroid use to increased mortality in common viper envenomation.

What to tell owners on the phone: no incision of the bite site, no ice, no tourniquet. Keep the animal still and get to a clinic.

Heat exhaustion and heat stroke

Israel in summer, so this is a constant. Cases here came more often from balconies and afternoon walks than from cars. Heat stroke kills fast — by the time you see signs of organ failure it is already late.

ConditionSigns
Heat exhaustionHeavy panting, hypersalivation, bright red mucous membranes, lethargy, seeking shade, mild weakness
Heat strokeCollapse, disorientation, seizures, vomiting or diarrhoea (± haemorrhagic), pale, brick red or cyanotic mucous membranes, tachycardia, loss of consciousness — emergency

Cooling — start before the full workup:

  • Cool, not ice-cold water — wet the body, focusing on neck, axillae, groin and paw pads
  • Fan over wet skin; evaporative cooling is the most efficient method available
  • Stop active cooling at a rectal temperature of about 39.5 °C, or you will overshoot into hypothermia
  • Never submerge an unconscious or seizing patient
  • IV fluids — they lower core temperature and treat the hypovolaemia at the same time
  • Oxygen supplementation

Monitoring: rectal temperature every 5–10 minutes during cooling. Then blood pressure, ECG for arrhythmias, blood glucose (hypoglycaemia is common), a coagulation panel for DIC, and renal and hepatic values. Acute kidney injury is a common and serious sequela — watch urine output.

Dogs cool by panting, not sweating. At 38 °C ambient, the air they are panting is already at body temperature and the system has nothing left. Brachycephalics start from behind.

Gastric dilatation and volvulus

GD is a stomach that fills with gas and distends. GDV is a stomach that fills and then rotates on its axis. GDV is the emergency: without surgery mortality approaches 100%, and with surgery survival is reported at 70–90% — time is most of that difference.

Who gets it: large and giant deep-chested breeds — Great Danes, German Shepherds, Irish Setters, Weimaraners — often after a large meal and exercise. But it happens in any dog.

Signs: non-productive retching, a rapidly distending abdomen, hypersalivation, restlessness, a weak rapid pulse and pale mucous membranes. Retching with nothing coming up is the single most telling sign.

Emergency approach:

  1. IV access and fluid resuscitation, immediately — two large-bore catheters if you can. Aggressive crystalloids, with colloids if needed. These dogs are haemodynamically compromised because the distended stomach compresses the caudal vena cava
  2. Analgesia
  3. Gastric decompression — attempt an orogastric tube. If it will not pass, trocarise through the abdominal wall to release gas. This buys time
  4. Confirm radiographically — the "double bubble" or "Popeye arm" on a right lateral view indicates volvulus
  5. Surgery — derotate, assess stomach and spleen viability, resect necrotic tissue, and perform a gastropexy to prevent recurrence

Post-operative: cardiac arrhythmias in 40–70% of cases in the first 24–48 hours, with ventricular premature complexes the classic finding — have lidocaine ready. Also watch for DIC, electrolyte derangement and hypotension.

GD is not GDV. Simple dilatation can often be decompressed and managed medically. The moment it twists, surgery is the only answer.

Gastropexy techniques

Gastropexy creates a permanent adhesion between the stomach and the body wall, either prophylactically in at-risk breeds or at the time of GDV correction.

There are five main described techniques. Worth separating what is described from what is actually done, because they are not the same thing:

Midline gastropexy is what gets performed — around 99% of the time. The ventral midline incision is closed together with the seromuscular layer of the stomach to the suture line (external rectus sheath). Everything below is the textbook list.
  1. Incisional — a 2–3 cm incision on the pyloric antrum and a partial-thickness incision on the transverse abdominal wall. The edge of the stomach is sutured directly to the body wall with a continuous pattern. The most commonly performed of the five.
  2. Preventative (incisional) — can be video-assisted laparoscopic. The stomach wall is grasped and pulled through a 3–4 cm incision behind the costal arch.
  3. Tube gastropexy — a feeding tube is placed through the body wall into the stomach. When the catheter is removed, scar tissue forms the permanent adhesion.
  4. Belt-loop — a seromuscular flap is raised in the pyloric antrum. A loop is made between the parietal peritoneum and the transverse abdominal muscle; the flap is passed through this tunnel and sutured back to itself.
  5. Circumcostal — as belt-loop, but the flap is passed around a rib to anchor it. Limited advantage over simpler methods given the increased risk of pneumothorax and rib fracture.

Gastrocolopexy — a further variant, fixing stomach to colon rather than to the body wall.

Whatever the technique, the goal is identical: a permanent, deliberate adhesion. Pick the one you can do well and quickly on a dog in shock.

3 · Reference notes

Things I looked up, was taught, or want to remember. Revision notes, not case work.

Oncology — CHOP and COP

Lymphoma is the most common haematopoietic tumour in dogs. The protocols differ by one drug:

DrugMechanism
C — cyclophosphamideAlkylating agent — cross-links DNA, so the cell cannot replicate
H — hydroxydaunorubicin (doxorubicin)Anthracycline — intercalates into DNA. The "H" that makes CHOP different from COP
O — Oncovin (vincristine)Vinca alkaloid — prevents spindle formation, so cells cannot divide
P — prednisoloneDirectly cytotoxic to lymphoma cells, and anti-inflammatory
  • Histiocytic sarcoma — dendritic cell origin. Breed predisposition in the Bernese Mountain Dog, Rottweiler and Flat-Coated Retriever. Can mimic haemangiosarcoma or lymphoma on imaging.
  • Furosemide in oncology — forced diuresis alongside nephrotoxic agents, and in the management of hypercalcaemia of malignancy.
  • Body surface area — BSA (m²) = 0.101 × weight (kg)2/3, used for chemotherapy dosing.

Neurology

  • SCRUBS - FIGGS — neurological exam acronym (need to flesh this out more).
  • Localise first. Hemiparesis, truncal sway and proprioceptive deficits — work out where the lesion is before building a differential list.
  • MUE (meningoencephalomyelitis of unknown aetiology) — an umbrella term for immune-mediated CNS inflammation, with GME, NME and NLE all sitting under it. Treated with immunosuppression. It does not reliably cause systemic fever.
  • Nerve compression is more common than blood vessel compression as a cause of lameness. Remember that when working through differentials.
  • A vasovagal response during cystocentesis or bladder expression is a real phenomenon, seen more often in cats.

Dermatology and ophthalmology

Canine pyoderma is primarily Staphylococcus pseudintermedius. Classification into surface, superficial and deep drives both the duration and the route of therapy.

  • Pathogens — Gram positive: S. pseudintermedius, S. aureus, Streptococcus canis. Gram negative: mostly E. coli.
  • Surface — pyotraumatic dermatitis ("hot spot"): acute, moist and self-inflicted, in hot humid weather and long coats. Skin-fold pyoderma: benzoyl peroxide, in brachycephalics and Shar-Peis.
  • Superficial — impetigo: juvenile pustular dermatitis, typically under 8–10 months, associated with ectoparasites, poor nutrition and poor hygiene. Superficial folliculitis: usually secondary to atopy, fleas or endocrinopathy, presenting as "moth-eaten" alopecia; chlorhexidine shampoo with systemic antibiotics.
  • Deep — beneath the follicle, into dermis and subcutis: canine acne, nasal pyoderma, pressure-point pyoderma, acral lick granuloma and generalised deep folliculitis.
  • Corneal ulcer → uveitis → IOP decrease. This is the chain. Uveitis will always drop IOP, unlike glaucoma, which raises it.
  • M. retractor bulbi retracts the globe. Blepharospasm indicates ocular pain.
  • Long-course glucocorticoids — protect the stomach and watch for gastrointestinal ulceration.

Drugs, labs and abbreviations

Drugs

  • Why ondansetron (Zofran) and not metoclopramide or maropitant? Maropitant (Cerenia) cannot be given to puppies under 16 weeks. Metoclopramide is a dopamine antagonist — fine, but it has CNS side effects. Ondansetron is a 5-HT3 antagonist, often preferred in vomiting with CNS involvement.
  • Amlodipine — calcium channel blocker, first-line for systemic hypertension in cats.
  • Pimobendan, furosemide and an ACE inhibitor — the classic congestive heart failure combination.

Labs

  • PCV and TS — the fastest bedside pair there is. Low TS with a normal PCV points to protein loss rather than blood loss.
  • cPLI — more specific than lipase for canine pancreatitis, but interpret it alongside imaging.
  • Creatine kinase — skeletal muscle, cardiac muscle and brain. Rises after trauma, seizures and prolonged recumbency.
  • SDMA — flags chronic kidney disease earlier than creatinine, at roughly 40% versus 75% nephron loss.
  • Lung ultrasound — A-lines are normal (air); B-lines indicate alveolar–interstitial fluid: oedema, pneumonia or haemorrhage.

Conditions I saw or was taught

  • Slipped capital femoral epiphysis — cats: obese, neutered, male, no trauma needed. Dogs: usually traumatic.
  • Multiple myeloma — two of four: monoclonal gammopathy, Bence Jones proteinuria, punched-out lytic bone lesions, marrow plasmacytosis >10%.
  • Hepatocutaneous syndrome — superficial necrolytic dermatitis with hepatopathy, with footpad lesions in older dogs.
  • Fever of unknown origin — CBC, biochemistry, urinalysis, cultures, imaging, and marrow if needed. Think infection, immune-mediated, neoplasia.
  • Hyperkalaemia — urinary obstruction is the classic cause and a true emergency. Look for ECG changes before the potassium result comes back.
  • Sialocele — accumulation of saliva in surrounding tissue; surgical resolution.
  • Bronchomalacia — airway collapse on expiration, with chronic cough in small breeds.
  • Intussusception — telescoping bowel, usually in young animals. A surgical emergency.
  • Protothecosis — algal infection affecting eye, skin, gastrointestinal tract and CNS. First time I had seen it. Difficult to treat, prognosis guarded.

Orthopaedic abbreviations from theatre

  • TPLO — tibial plateau levelling osteotomy, for cranial cruciate disease
  • TTA — tibial tuberosity advancement, for cranial cruciate disease
  • CCWO — closing cranial wedge osteotomy
  • PLO — patellar luxation osteotomy
  • TECABO — total ear canal ablation + bulla osteotomy. Need to read more on this one.
  • Hemivertebrae — visible radiographically, especially in screw-tailed breeds, and a cause of spinal cord compression

Open questions I'm still working through

Written down deliberately. These are what I want to ask about on the next rotation.

  • Recurrent disc herniation — how do you manage a dog through repeated IVDD episodes, and where is the line between conservative management and surgery?
  • A patient on glucocorticoids that develops CNS signs — the answer depends on whether the steroid is the cause or the treatment, but how do you decide quickly at three in the morning?
  • ICU flow sheets: the centre used a digital system for real-time vitals, medications and treatments. I want to learn one properly before my next critical care placement.

4 · Reflection

The pace is relentless. By week two you have a rhythm; week one is simply overwhelming. The specialists here are exceptional and genuinely want to teach — if you ask questions they will stop what they are doing to explain. If you don't ask, they assume you know.

What I'd do differently. Review the specialty of the week in advance. If it is neurology week, re-read the neurological examination the night before. And speak to the department head at the start of each week — they will tell you what is coming in and what to look out for.

The other thing I'd change is this document. I wrote most of it between cases on my phone, and it showed. Next rotation I'm keeping a structured log from day one — signalment, presentation, working diagnosis, outcome, and one thing learned — so the write-up is a by-product rather than a weekend of reconstruction.

The network I built here — residents, specialists, students from other schools — is the part I'll carry forward. Medicine in a referral setting is genuinely collaborative.