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Approach to the depressed/recumbent foal (Diagnostic approach (Thorough…
Approach to the depressed/recumbent foal
Physiological differences between foals and adult horses (important for therapeutic consideration)
Larger total body water (TBW) content and ECF volume.
Susceptible to water loss due to high SA:V and kidneys are less able to compensate.
Hepatic immaturity (slowed drug metabolism, but normalises by about 1 mth)
Antibiotic doses usually higher than adults, and may have shorter dosing interval
Susceptible to derangements in blood glucose and electrolytes (immature homeostatic mechanisms)
Agammaglobulinaemic at birth and deficient components of innate immunity (Ab levels and neutrophil function depends on passive transfer)
Prone to Na overload when giving Na-rich fluids
Intensive care & stabilisation of the critical foal
CVS support and oxygentation
Jugular catheterisation (+ collection for culture/lab testing) and pre-warmed Hartmann's (20 ml/kg/20 mins - max. of 4 L). If uroperitoneum (confirmed by AFAST, abdominocentesis and serum biochem), then use 0.9% NaCl.
IF UROPERITONEUM: Ca gluconate (protects myocardium), glucose +/- insulin (drives K into cells) and if severe then NaHCO3 (drives K into cells and corrects acidosis).
Maintenance fluids: should usually be low sodium (unless diarrhoea or renal compromise as in SIRS) such as combined 10% glucose and Hartmann's (run from separate bags into same line).
Electrolytes rarely needed (usually correct with fluids), but should be supplemented as required.
Supplement fluids with 10% glucose (5 mg/kg/min).
Intranasal oxygen (if tachypnoea, dyspnoea, cyanosis, restlessness, or SaO2 < 90%).
Antimicrobial therapy
Indicated in septic/compromised foals.
Broad-spectrum bactericidal, instigated pending culture results.
IV pen/gent if normal renal function (large doses of gent required in neonates). If renal compromise: TMS, ceftiofur or ticarcillin/clavulanic acid.
Anti-endotoxic therapy
Flunixin (not if renally compromised, dehydrated or hypovolaemic).
Ongoing care of the critical foal
Umbilical care
Dip umbilicus in iodine BID for first three days (or until standing).
PO TMS or doxycycline if infected.
U/S evaluation of umbilical remnants.
If patent urachus: PO broad-spectrum antibiotics with clean. dry environment. Usually resolves with medical therapy within days.
Musculoskeletal support
Refer to ALDs/orthopaedic conditions notes
Analgesia
If flunixin contraindicated, butorphanol commonly used.
Diagnostic approach
Thorough history
High-risk pregnancy (e.g. placentitis)?
Standing/sucking behaviour at/after birth? Foals should stand within 1 hr and suck within 2 hrs.
Time since birth?
Foaling environment?
Mare gestational vaccination: strangles/tetanus 4-6 wks prior to foaling, and EHV-1 at 5, 7 & 9 mths of gestation.
Dystocia?
Appearance of foetal membranes?
Meconium passed (i.e. evidence of "milk dung")?
Onset/progression of clinical signs?
Physical examination
Vitals
Normal parameters (up to 12 hrs old)
HR 110-120, RR 40, Temp 37.8.
Normal parameters (up to 24 hrs old)
HR 90-100, RR 30, Temp 37.8.
Hypoperfusion signs
Depression, tachycardia/bradycardia, MM pallor, poor CRT/jugular refill, poor pulse quality, oliguria, ileus, cold extremities/shivering.
Endotoxaemia signs
Depression, injected MMs, prolonged CRT (hypotension), colic signs (abdominal pain, tachycardia, ileus), core temperature derangement, cool extremities, +/-haemorrhage (internal/external), icterus, anorexia, laminitis.
Gut sounds
Assess for ileus.
Look for septic foci
Assess for evidence of trauma (e.g. wounds with drainage).
Palpation of the joints (heat, pain, swelling), umbilicus (pain, heat, swelling), opthalmic exam (uveitis)
Rectal palpation
Assess for meconium impaction.
Abdominal ultrasound
Assess for peritoneal fluid, ileus/gaseous distension of intestine (+/- impaction), and pathology of the umbilical remnants (Ultrasound of umbilical structures (widened umbilical stump, thickening of urachal/vessel walls, luminal dilation/fluid accumulation, gas shadows, abscesses).
Blood sampling
Serum [IgG]
Haematology and biochemistry (assess for haemoconcentration, inflammation, SIRS/MODS, electrolytes etc.)
Blood culture (esp if signs of sepsis) -
Radiography
Particularly thorax and joints (look for evidence of pneumonia or osteomyelitis).
Faecal sampling (if diarrhoea)
FEC, faecal culture +/- PCR or Clostridium toxin assay
Abdominocentesis
Normal peritoneal fluid: straw-coloured, TP < 25 g/L, < 3000 cells/μl, lactate < 1 mmol/L, some neutrophils.
Uroperitoneum: unless UTI, urine causes a sterile peritonitis and production of exudative effusion (cloudy, turbid to flocculent, TP > 25 g/L, NCC > 5 x 10^9/L). Compare fluid and serum creatinine levels (2x higher or greater in fluid is diagnostic).
Septic peritonitis: exudative effusion (as above) + degenerative neuts/toxic change and phagocytosed bacteria on cytology.
Aseptic synoviocentesis
Normal synovial fluid: clear-yellow, viscous. NCC < 0.45 x 10^9, neuts < 10%, TP < 20 g/L.
Septic arthritis: serosanguinous, watery (+/- clots). NCC 20-150 x 10^9, neuts > 90%, TP 30-60 g/L.
DDx
Immunodeficiency disorders
Sepsis
Aetiology
Typically Enterobacteriaceae (E. coli, Klebsiella, Enterobacter, Salmonella) and Staph/Strep. Common infection sites include the placenta in utero, gut (prior to closure), umbilicus and respiratory tract.
Risk factors
Maternal: placentitis, systemic illness, stress, loss of colostrum, poor nutrition, prolonged gestation.
Foal: prematurity/dysmaturity, FPT (complete or partial), NMMS (weakness/delayed nursing), suckling prior to cleaning mare's perineum/udder, focal infection, neonatal isoerythrolysis.
Environment: poor foaling/stable hygiene.
Pathophysiology
After invasion, SIRS is initiated and may predominate over CARS. Bacteria typically establish septic foci in GIT, joints, lungs, eyes, brain, liver and kidney. Septic arthritis and bacterial meningitis may ensue.
Clinical signs
Variable. Anorexia, depression (+/- seizures), recumbency, tachycardia, tachypnoea/dyspnoea, lameness, abdominal distension, diarrhoea. Assume septic until proven otherwise!
Therapy
Antibiotics
Initially pen/gent (can use TMS if renal compromise). Later adjusted according to culture/sensitivity. 2 week therapy unless focal infection.
Fluid therapy
Resuscitative: 20 mL/kg (1 L) bolus over 20 mins. Max 4 L. Signs of hypoperfusion after 3 L: consider dopamine.
Maintenance: low-Na fluids (e.g. 10% glucose + Hartmann's) at 94-240 mL/hr. Maintenance is 94 mL/hr. Supplement electrolytes (KCL, MgSO4) and glucose as required.
Supportive care
Joint lavage (reduces bacterial load - 3-5 L pre-warmed Hartmann's per joint)
Colostrum/plasma if FPT. Plasma indicated if FPT and foal > 12 hrs old.
Clean, dry bedding, catheter management, opthalmic management (corneal ulcers), frequent repositioning (pressure sores).
Diagnosis
Sepsis scoring: not very accurate but uses multiple clinical factors to determine whether sepsis may be occurring.
Blood culture (gold standard): lag time not ideal, often treated based on clinical presentation. Culture may be performed using samples from other septic foci (e.g. synovial fluid).
Haematology/biochem: leukopaenia (+/- toxic change and left shift), high SAA (first 12-24 hrs) and/or fibrinogen (first 36 hrs), hypoglycaemia, azotaemia, metabolic acidosis. High serum [lactate].
Additional tests: thoracic radiographs, synoviocentesis, arterial blood-gas, ultrasound of umbilical structures (assess for thickness, presence of gas and/or rupture), faecal culture/PCR.
Physical exam: septic foci, tachycardia/tachypnoea, MM petechiae/scleral injection, poor pulse, prolonged CRT/jugular refill, cool extremities, ileus, decreased urine output. Temp not a good indicator of sepsis.
Serum [IgG]: FPT if < 8 g/L (partial if > 4 g/L).
Neonatal isoerythrolysis
Risk factors
Many must coincide: stallion with Aa RBC antigen + mare without Aa alloantigen, intrauterine infection/pathology (exposure of foetal blood to mare) or dystocia (repro tract trauma exposing mare to foetal blood).
Aetiology
Stallion must have Aa RBC Ag, and covers a mare without Aa alloantigen. Foal inherits Aa RBC Ag, mare is exposed to foal blood and develops antibodies directed against foal RBCs.
Pathophysiology
Occurs in first week of life. Foal ingests sensitised mare's colostrum and antibodies directed against its RBCs. IVH (+ accelerated EVH) ensues, causing anaemia and icterus. May lead to bilirubin encephalopathy & CNS hypoxia (seizures). Death from anaemic hypoxia may occur.
Clinical signs
Foals initially healthy/nurse normally, but develop icterus, tachycardia/tachypnoea, Hburia, lethargy and weakness within 24-72 hrs. Anaemia + pigmenturia = IVH.
Diagnosis
Clinical signs & signalment (icterus, anaemia, pigmenturia)
Minor cross match (mare serum or colostrum + washed foal RBCs): agglutination indicates NI.
Therapy
Immune support: foals often febrile and sepsis is difficult to rule out. Treat with pen/gent, or TMS if renal compromise.
Blood transfusion (not always required): If PCV < 12% or if rapidly falling. Start at 20 mL/kg and increase rate if tolerated. Ideal donor is the mare (use her washed RBCs - NOT HER SERUM) - her RBCs won't react with her Abs inside the foal.
Immediately restrict udder access: muzzle foal. After 36 hrs the mammary gland stops producing colostrum and the foal cannot absorb alloantibodies, so can suckle from then on.
Fluid therapy: maintenance 94 mL/hr + deficit and ongoing losses. Replace deficit over 12 hrs. Addresses dehydration and prevents nephrotoxicity of Hburia.
Rest and general supportive care (warmth, stress minimisation).
NMMS
Risk factors: maternal/placental disease, twins, premature/dysmature, umbilical cord compression, dystocia, isoerythrolysis .
Aetiology: describes a variety of non-infectious neurologic signs in the immediate postpartum period (doesn't assume a specific process). Encompasses ischaemic/hypoxic events (HIE, PAS) and non-ischaemic events (metabolic, endocrine or NT imbalance).
Pathophysiology: ischaemia may occur due to placentitis, dystocia, isoerythrolysis etc. They predominantly affect organs such as the heart, kidneys, GIT and liver. Non-ischaemic events are less defined, and may be due metabolic, endocrine or NT imbalance (e.g. chronic foetal stress impairs brain development). Foals are more susceptible to FPT and sepsis due to abnormal behaviour.
Clinical signs: disorientation, wandering, abnormal udder seeking/sucking on objects, seizures, tremors, star gazing + other CNS signs.
Diagnosis: ruling out of infectious/congenital conditions, clinical history and signs.
Therapy: general support - seizure control, oxygenation, fluids, nutritional supplementation (+/- colostrum/plasma), control of concurrent disease/infection.
Uroperitoneum
Risk factors
NMMS, dystocia, prolonged recumbency, umbilical infection, meconium impaction.
Aetiology
Ruptured bladder most common, but also ruptured urachus. Typically due to trauma during parturition.
Pathophysiology
Urine in the abdomen leads to aseptic peritonitis. Diffusion of urine across the peritoneum causes hyperkalaemia, hyponatraemia and hypochloraemia (urine is low in Na and Cl so has a dilution effect). To compensate, renal excretion of potassium increases in exchange for hydrogen ion retention (acidosis).
Diagnosis
Physical exam: abdominal fluid wave and clinical signs.
Haematology/biochem: hyperkalaemia, hyponatraemia, hypochloraemia, metabolic acidosis (increased AG and decreased HCO3)
AFAST: presence of peritoneal fluid.
Abdominocentesis: peritoneal creatinine : serum creatinine > or equal to 2:1 is diagnostic.
ECG
Clinical signs
Straining to urinate, lethargy, abdominal distension, tachycardia/tachypnoea, poor pulse, hypovolaemia, CNS signs and cardiac arrhythmias (hyperkalaemia).
Therapy
Gradual abdominal drainage (indwelling catheter)
Fluid therapy: 0.9% saline
If severe hyperkalaemia: Ca gluconate (protectsmyocardium), dextrose + insulin (shifts K intracellularly) and NaHCO3 (only if very severe).
If peritonitis: pen + gent + metronidazole
Eventual surgical repair of bladder (+/- removal of umbilical remnants) and peritoneal lavage.
Meconium impaction
Risk factors: PAS, postmature foals, Thoroughbreds,FPT, sepsis
Aetiology: usually passed within 12 hrs. Impactions typically occur in the small colon. As colostrum is a laxative, many cases suffer from FPT.
Pathophysiology: impaction leads to ileus and gaseous distension, and may compromise the intestinal mucosa leading to sepsis.
Clinical signs: tachycardia, tachypnoea, anorexia, mild to severe colic, recumbency with rolling, straining to defecate, tail swishing/lifting, squatting, crouching, abdominal distension.
Diagnosis
History (passed faeces/"milk dung"?).
Digital rectal exam: may feel pellets of meconium/impaction.
Abdominal ultrasound: gaseous distension, may see impaction.
Therapy
Enema: best is warm, soapy water
NGT paraffin oil if refractory to enema
Fluid therapy
Analgesia (avoid NSAIDs): butorphanol common
Diarrhoea
Risk factors: NMMS, FPT, sepsis, antimicrobial therapy
Aetiology
Physiological: "foal heat" diarrhoea. Foal will be clinically well, no fever.
Dietary: milk overload, inappropriate milk replacer. Foal will be clinically well, no fever.
Bacterial: clostridium (most common), salmonella (zoonoses), R. equi. Salmonella and Clostridia are invasive and cause sloughing of mucosa (haemorrhagic) and malabsorptive + secretory diarrhoea.
Viral: rotavirus (often dehydrate quickly) causes malabsorptive diarrhoea.
Protozoal: cryptosporidium parvum (zoonotic) - often self-limiting.
Parasitic (uncommon): Parascaris equorum (usually other signs of ill-thrift).
Pathophysiology: multiple mechanisms. Clostridium and Salmonella are most common agents, especially with antimicrobial therapy. Alterations in fluid and electrolytes may be life threatening, and invasive agents bay predispose to sepsis.
Clinical signs: anorexia/ill-thrift, perineal staining, dehydration, sepsis, diarrhoea
Diagnosis
History (focus on sucking behaviour and nutrition)
Faecal samples for virology testing, bacterial culture, PCR, clostridial toxin assays, and microscopic examination.
Blood culture (as with sepsis)
Haematology and biochem: haemoconcentration, azotaemia +/-signs of sepsis
Therapy
Fluid therapy: if PO, ensure electrolytes and glucose. Give 500 mL q1-2h. If IV, can give 1L bolus over 20 mins for resuscitation and then decreased to 94 mL/hr (3-5 mL/kg/hr).
Antibiotics: often prophylactic to prevent sepsis (IV TMS in dehydrated foals). Hydrated foals can be given pen/gent or TMS.
Nutritional support: +/- indwelling feeding tube. Do not withhold milk if foal wants to suck.
Prematurity/dysmaturity/IUGR
Risk factors: IUGR (maternal/placental disease), twins, induced parturition
Aetiology
Premature: born < 320 days.
Dysmature: immature body systems (not necessarily premature)
Pathophysiology
IUGR caused by maternal (systemic disease, starvation), placental (inflammation, thrombosis, umbilical obstructions, endometriosis) and foetal (twins, congenital abnormalities) factors.
Clinical signs
Emaciation, abnormal skeletal development, small size for gestational age, domed head, floppy ears, short silky coat etc. Predisposed to other conditions such as FPT and sepsis.
Diagnosis
History and clinical signs
Therapy
Intensive care/supportive therapy, especially treatment of secondary disease (e.g. sepsis)
Parasitism
Aetiology
Strongyloides westeri (threadworm)
Parascaris equorum (round worm)
Clinical signs
Ill-thrift, diarrhoea
Pathophysiology
P. equorum is most significant in foals < 6 mths (immunity usually develops after 6 mths, and immunity to threadworm develops at approx. 3 mths). They are ingested, then migrate across the gut wall to the liver and lungs. After development, they are coughed up and swallowed. They undergo their final maturation in the intestine, and eggs are released in faeces. Liver and lung damage can occur. Immunosuppression may lead to other diseases, esp. R. equi bronchopneumonia.
Diagnosis
FEC
Treatment/prevention
Benzimidazoles most effective against P. equorum