Note that neonates are not miniature adults!

•   rapid changes in clinical condition – avoid delays in treatment

•   clinical signs are subtle - only recognised by those with knowledge of normal behaviour

•   multiple organ involvement common

•   high risk of life threatening infections due to immuno-incompetence - so hygiene and aseptic

  technique are very important 

0. Take history to determine whether foal has risk factors for developing neonatal problems:

•   Maternal conditions - sick mares, past history of problem foals

•   Parturition problems - immaturity, prolonged labour, early cord rupture, caesarean

•   Foal conditions - meconium staining of foal (indicates prepartum foetal distress), placental

  abnormalities, twins, orphans, premature or dysmature foals

•   Abnormal post partum behaviour - Within 5 min of birth, cord should rupture and shivering,

  sucking (check with finger) & righting reflexes should develop. Assess time foal took to stand

  (normal<2h), suck (<3h), urinate (<8h) and void meconium (12-24h).

•   Is foal premature or dysmature? Mean gestation is 341 days (315-365 days). Premature = <

  320 days. Dysmature = > 320 days but has functional immaturity - may follow in utero infections, twins (even if one resorbed), placentitis. Signs of prematurity/dysmaturity include weakness, delay in standing, poor sucking, low birthweight, soft skin, hair and hooves, domed head, lax fetlock joints, floppy ears, red tongue, reduced thermoregulation (susceptible to hypothermia), incomplete ossification of carpal and tarsal bones, tachypnoea and respiratory distress. 

• Temp <38oC

•   Pulse 80-120/min;

•   Resp rate (30 - 40/min), 

0. since multiple organ/system involvement common

   •   Demeanor; assess alertness & behaviour towards mare. Remember foals normally spend

     considerable time sleeping, but should stand up & suck when you enter stable!

   •   Temp <38oC

   •   Pulse 80-120/min;

   •   Resp rate (30 - 40/min), normally have a small abdominal component.

   •   Eyes; suture lines & persistent hyaloid artery common. Check for ulcers, uveitis (usually

     indicates septicaemia), congenital lesions (cataracts), entropion. PLR usually slow.

     Menace response absent until 2 weeks old.

   •   Mouth; Visualise and palpate hard palate/soft palate if possible. Check sucking.

   •   Nostrils; Milk at nostrils caused by (a) cleft palate (b) pharyngeal paralysis (c) temporary

     pharyngeal dysfunction especially in weak foals.

   •   Mucous membranes: As for adults, but usually pinker. Petechial haemorrhages confined

     to the sclerae are common result of birthing trauma. Generalised petechiation suggests septicaemia or thrombocytopenia. Icterus commonly due to septicaemia > neonatal isoerytholysis >> hepatitis, fasting, physiological icterus.

   •   Respiratory system; Normal breath sounds are louder than adult because of thin chest wall. Adventitious sounds commonly audible over ventral lung fields soon after birth - due to aspiration of fluids or atelectasis – resolve within hours. Correlation between lung sounds and lung pathology is poor in foals – absence of adventitious sounds does not mean there is no significant lung pathology - can have considerable consolidation and/or interstitial disease without abnormal sounds. Coughing and nasal discharge are rare in neonates with lung disease - tachypnoea/dyspnoea more common.

   •   Cardiovascular; Commonly hear pansystolic (Grade I-IV) murmur at cranial left heart base for up to 7 days - due to PDA or functional murmur. Palpate thorax for fractured ribs (common).

   •   Abdomen; Interpret borborygmi as for adults. Palpate umbilicus & scrotum - testes usually descended. Ballot for fluid thrill which usually indicates uroperitoneum. Abdominal distension – differential diagnosis includes intestinal obstruction, overfeeding, enteritis with gas production, uroperitoneum. Perform gentle digital rectal examination if uncertain if

     meconium is voided. Meconium staining on coat indicates in utero stress.

     •   Musculoskeletal; Assess gait, tendons (weak especially if immature), flexural and angular

       limb deformities, joints and physes for evidence of infection.

     •   Neuro examination; As for adult, except menace response absent in neonate. NB foals

       often ‘twitch’ when being restrained during examination – do not misinterpret this as a

       seizure.

     •   Haematological and biochemical examination – use reference ranges for analytes in foals

       as they often differ from those of adults. 

      

• Resuscitation – ABC as for small animals.

•   Control seizures with diazepam (5-20mg slow IV to effect)

•   If hypothermic (<37oC) provide heat lamp or blankets – don’t forget energy!

•   Check blood glucose (Glucometer) - if <2.2 mM administer 0.08 ml/kg/min 10% glucose

  solution IV until blood glucose normal. Recheck frequently.

•   Assess hydration status and, if possible, acid base balance and administer fluids as required

  via indwelling IV catheter (asepsis is very important).

•   Collect blood for routine haematology (EDTA tube), fibrinogen (Na citrate tube), IgG

  electrolytes, urea and creatinine (plain tube).

•   Collect blood aseptically for blood culture (10ml heparinised) -> blood culture vial.

•   Treat navel with 0.05% chlorhexidine if moist - repeat for several days

•   Give tetanus antitoxin if mare not vaccinated within last 4-6 weeks of gestation. Lasts approx

  3 months - then vaccinate as normal >3 months. 

•   ensure adequate colostrum – frozen, commercial freeze dried or milked from dead mare.

•   get foster mare if possible - (Foal bank 01952-811234).

•   Powdered milk e.g. FoalLac – used as indicated on tub. 

0. FAILURE OF PASSIVE TRANSFER OF ANTIBODY (FPT)
   

0. Incidence – probably ~10% foals. Higher on some premises.
   Cause – mostly failure to suck
   Detection - Measure neonatal serum IgG from 8-24h onwards. Cannot do when >2 weeks since foals own IgG production will affect results. Single radial immunodiffusion kits - most accurate, highly specific, but time consuming (18-24 h) and expensive. CITE test - accurate and suitable for field use. Normal IgG at 24 h old >8 g/l. FPT is partial (4-8 g/l), or complete (<4 g/l). Partial FPT may not need treatment if foal is clinically normal and in clean environment. Treat complete FPT (<4 g/l) otherwise foal susceptible to sepsis. 

0. FAILURE OF PASSIVE TRANSFER OF ANTIBODY (FPT)
   

   Treatment 

0. Treatment:

•   <24h old foals - 1-2L colostrum PO (bottle preferred to nasogastric intubation). Remember –

  milk contains negligible IgG by 24h post-partum so collect it during first 4-6h. Lasts in freezer

  for 12 months. Bovine colostrum suitable in emergency.

•   >24h old foals. Intestinal absorption of IgG ceased so give 1-2L equine plasma IV. First litre

  over 60+ minutes and slower rate subsequently. Rare complications include tachypnoea, shivering, anaphylaxis, volume overload - if encountered slow infusion - if persistent stop infusion. Most common to use commercial plasma - from universal donors. Approx £150/L. Alternatively collect plasma using blood transfusion kit - from universal donor if available – if not collect from stallion or gelding (less chance of having anti-RBC antibodies than multiparous mares). Plasma separated by gravity and transfused into foal. Cross matching rarely done - adverse reaction to first transfusion extremely rare. 

0. Prevention of FPT; Good nutrition of pregnant mares. Mares on premises >2 weeks prepartum, so produce antibodies to pathogens in foaling environment. Minimise stress. Careful observation (but minimal interference) of dam/neonate during first 24h. Ensure adequate colostral intake during first 12h - supplement early if necessary. Careful attention to premature/weak neonates. Store quality frozen colostrum. Measure colostral quality. 

An immune mediated haemolytic anaemia. Destruction of foal's RBCs by colostral antibodies which are directed against foal's RBC membrane alloantigens. Horse has >30 erythrocyte alloantigens, but most (>90%) incompatibilities are due to alloantigens Aa and Qa. Problem occurs when foal inherits Aa or Qa alloantigens from Aa or Qa + ve stallion and when RBCs of mare are negative for these antigens - during birth of this foal, foetal blood often leaks into maternal circulation – and mare makes anti Aa or Qa antibodies.

As antibodies peak at 9 days after foaling they are not transferred in colostrum at first pregnancy - thus do not get NI in first partum mares. However in subsequent pregnancies mare produces increasing amounts of these antibodies which are excreted in colostrum - if subsequent foals are Aa or Qa positive these antibodies cause NI. 

Clinical signs; Normal at birth, signs begin from 6-48h. Anaemia with weakness, icterus and rarely haemoglobinuria, depression, anorexia, progressing to collapse and death.
Diagnosis; Clinical signs and history are usually sufficient. Can use cross match (rare). 

Treatment; Prevent further absorption of mare’s colostral Ig – give alternative milk until foal is >24h old. Milk mare thoroughly and regularly and discard colostrum. Blood transfusion required if PCV <10-12% or if PCV reducing rapidly. Can transfuse thoroughly washed RBCs from mare - wash 3 x in saline, then administer 1-2l of 50% suspension of RBCs in saline. Alternatively transfuse whole blood from Aa, Qa alloantigen negative horse (or if cannot test use blood from stallion or gelding that has never had a transfusion). Collect blood into transfusion bags as plasma, and administer whole blood via inline filter - give 1-2 l of blood at 1 l/hour. Latter is most common approach. Monitor clinical and RBC parameters over following days. May require repeat transfusion as donor cells are destroyed quickly.

Prevention If possible, don't mate Aa or Qa -ve mares with Aa or Qa +ve stallions. Test at risk mare's serum for alloantibodies - in last 2 wks of gestation when levels are increasing. If +ve then must prevent foal sucking that mare. And feed alternative colostrum 

IMMUNODEFICIENCY DISORDERS 

Fell pony syndrome, Combined immunodeficiency syndrome (CID) (see Congenital, hereditary, immunologic and toxic disorders lecture) 

The major cause of neonatal mortality. Prognosis guarded. Prompt therapy critical for success. Portal entry GIT, lung, umbilicus, iatrogenic
Aetiology: Rarely acquired in utero - if so are sick at birth. Most acquired post-partum - signs develop after 48-96h. Bacteria are usually ubiquitous environmental bacteria - mainly Gram -ve (E. coli, Salmonella, Klebsiella, Actinobacillus, Pseudomonas, Enterobacter) and less often Gram +ve (Streps, Staphs, Rhodococcus equi, Clostridia).

Sites of sepsis - lungs > bones and joints > GIT
Signs: Initially have non-specific signs; reduced appetite, decreased sucking, dullness, increased recumbency, pyrexia. Rapid progression to signs of MULTISYSTEM involvement - meningitis, diarrhoea, colic, tachypnoea, resp distress, lameness, swollen joints, omphalophlebitis, uveitis, petechiae, scleral injection. By the time these clinical signs develop, the disease is well advanced. Diagnosis: Blood culture (not 100% sensitive). History and clinical signs alone not very accurate. Compute sepsis score (several scoring systems available) based on weighted clinical and lab findings - gives probability of foal having sepsis. 

• Blood or body fluid cultures (transtracheal aspirate, synovial, peritoneal and pleural fluid) very useful. Collect samples before administration of antibiotics, ideally when foal is pyrexic. Do not collect blood from indwelling i/v catheter since may have surface contaminants. To prevent culturing skin contaminants, clip hair, prepare skin aseptically, soak in alcohol for 30s, sterile gloves and syringe, use different needle for puncture and for introducing blood into bottle. Do aerobic and anaerobic cultures. False negative rates - 10-25%. Also worth doing gram smear on body fluids, as this may provide immediate info on type of bacteria, and aid selection of antibiotic.

•   Haematology- WBC counts may be normal, increased or decreased depending on stage of infection - may need to follow progress of counts (serial evaluation). Presence of band and toxic neutrophils is suggestive of sepsis. Septic foal are often thrombocytopenic.

•   Fibrinogen increased after 24-24h

•   IgG may be low

•   Hypoglycaemia, low PaO2, metabolic acidosis 

• Antibiotics - While awaiting culture results, use broad-spectrum antibiotics e.g. penicillin plus gentamicin, ceftiofur or cefquinome. Change therapy if necessary after culture and sensitivity results obtained (2-4 days). Treat for >1-2 weeks after clinical signs of sepsis have resolved - often need antibiotics for 1-2 months especially if persistent infection.

•   Local therapy eg joint lavage, pleural drainage, umbilical surgery etc

•   IgGs - May need supplementing since many will have FPT 

Common - 70-80% of foals affected. In contrast to adults, most diarrhoea reflects SI disease, since colon cannot compensate until >3 months. Aetiology should be determined if likely that is herd problem or if potential zoonosis - submit faeces (salmonella, rotavirus, cryptosporidium, parasites) and blood culture (if suspect septicaemia). 

• Foal heat diarrhea 

• common. Occurs at 6-14 days. Due to alteration in colonic microflora and epithelium as they adapt from milk to grass diet and perform coprophagy. Not milk oestrogens as once thought - since occurs in orphaned foals. Transient (2-4d) self curing diarrhea. No Rx required but watch in case it isn't foal heat diarrhoea - reconsider diagnosis if becomes ‘sick’ (pyrexia, depression, dehydration, anorexia etc). 

• Nutritional diarrhea; 

• overingestion of milk (common when mares are on lush grass) causes protein and CHO to pass into LI causing osmotic diarrhoea. Also with diet change. 

• Rotavirus; 

• main cause foal diarrhoea (30-60% cases). Widespread in equine population (100% adults have titres). Adults probably source for foals. Survives for >9 months in environment. Many foals <1 month die, foals >1 month mild enteritis only. Profuse watery, non foetid diarrhoea, depression. Mainly affects small intestine - stunting of villi + loss of absorptive capacity together with increased intestinal secretion. Diagnosed using ELISA or latex agglutination - submit faecal sample. Treat with specific antisera orally or treat symptomatically (fluids). Avoid overstocking. Vaccinate mare in 8, 9, 10th month of gestation with inactivated equine rotavirus (Duvaxyn R), to provide colostral protection. 

• Salmonellosis; 

• Mare is most likely source. Commonly mild enteritis but may cause severe septicaemia. Enteritis present either as foetid diarrhoea or with colic prior to onset of diarrhoea. Salmonella rare as a cause of chronic diarrhoea. 

• Clostridium perfringens types A B & C; 

• causes foetid necrotising haemorrhagic enteritis in 1-2 day old foals - commonly causing death within 48h. 

• Septicaemia; 

• diarrhoea is common presenting sign in septicaemia. 

• Aeromonas spp 

•  probable primary cause of diarrhoea in foals. 

• Escherichia coli; 

• significance unclear - no specific pathogenic serotypes for foals 

• Coronavirus and adenovirus; 

• uncertain pathogenicity. 

• Cryptosporidium;  

• unclear significance. Diagnose by visualizing oocysts in faeces. Only

  symptomatic therapy. Zoonosis. 

• Strongyloides westeri; 

• Significance unclear; probably doesn't cause diarrhoea per se, but

  may contribute to dysfunction in conjunction with other pathogens. Mare's milk is major source to foal - egg output 2-3 wks after parturition. Rx – anthelmintics (not moxidectin!) 

• Fluid therapy; critical since likely have dehydration, metabolic acidosis, and reduced Na, Cl, K. For mild dehydration administer isotonic electrolyte solutions orally, little and often. Severe dehydration usually requires IV fluids.

•   Antibiotics; controversial and probably overused. Not indicated in nutritional, viral and parasitic diarrhoea. Only give in foals <1 month old if suspect bacterial disease since bacteraemia likely at this age, and in foals with FPT.

•   Adsorbents; Bismuth subsalicylate (Peptobismol), diarsanyl and Biosponge may help. Activated charcoal and kaolin/pectin less useful.

•   NSAIDs; reduce endotoxaemia and attenuate abdominal pain - care as risky due to toxicity - GDU and renal papillary necrosis especially in dehydrated foals.

•   Codeine; only if severe, profuse diarrhoea.

•   Plasma; if have FPT or use rotavirus hyperimmune sera orally

•   Live yoghurt, probiotics - good. Alternatively give mare’s faeces orally to foal

•   Antiulcer therapy given routinely in most instances

•   Nutrition - if moderate diarrhoea keep on mare’s milk. If milk causes bloat or colic give

  electrolyte solutions - however if on these solutions for >1 day get undernutrition - consider

  supplemental parenteral nutrition

•   Hygiene - important to limit spread to other foals or zoonosis

•   Nursing - clean and dry perineum and cover with Vaseline/ZnO to prevent scalding 

APPROACH TO FOAL WITH ABDOMINAL PAIN 

APPROACH TO FOAL WITH ABDOMINAL PAIN

Differentiation of medical versus surgical colic presents a diagnostic challenge - similar basis to adult except, (a) cannot do rectal (except digital exam for meconium retention and for diarrhoea), (b) abdominal radiography, ultrasound, palpation and blood gas - acid base analysis and gastric endoscopy are more useful than in adult. Treat mild non-surgical abdominal pain with low dose phenylbutazone or flunixin.

•   gastroduodenal ulceration

•   meconium impaction

•   impending enteritis - preceding diarrhoea

•   obstructive GIT lesion - most congenital atresia presents <36h of birth

•   uroperitoneum (only mild pain)

•   peritonitis - ruptured ulcer (rare)

•   traumatic damage - stood on by mare (rare)

•   Tyzzer's disease (rare) 

0. GASTRODUODENAL ULCERATION (GDU) 

   aetiology 

0. Probably multifactorial. Stress important – consequently most sick foals are given GDU prophylaxis. Iatrogenic - foals susceptible to NSAID toxicity - inhibit PG synthesis causing gastric mucosal vasoconstriction and ischaemia. Infections - proposed cause as get clusters of GDU on certain studs. 

0. GASTRODUODENAL ULCERATION (GDU)

   signs  

0. Most foals have a few ulcers on non-glandular side of margo plicatus without symptoms. Symptomatic ulcers occur from day 1 onwards causing anorexia, salivation, colic after sucking (rolling, dorsal recumbency, odontoprisis, "tongue-sucking"), regurgitation of mucoid/watery gastric fluid at nares. Rarely develop perforating ulcers - severe peritonitis and most die in a few hours. 

0. commonly diagnosed based solely on clinical signs and response to therapy. May perform endoscopy (withhold solids 12h, milk 4h before).
   

0. Proton pump inhibitor (omeprazole) most effective and most commonly used. 

0. Meconium usually voided within few hours. Retention mainly in males due to narrow pelvis. 

0. Signs: start 6-24h - restless, straining, lifting tail, rolling, lying on back, attempts to urinate. Straining may reopen urachus - drip urine in conjunction with straining.
   

0. Rx: warm soapy water as enema using SOFT tube inserted 10-12" and gravity flow. Forceps or rectal spoons NOT recommended. IV fluids rarely required. If non-responsive use 200ml liquid paraffin or dioctyl 10ml 5% solution in H2O by stomach tube. Analgesia as required. Very

   occasionally need surgical intervention. 

0. TYZZER’S DISEASE 

0. Uncommon in UK - infectious necrotic hepatitis caused by Clostridium piliformis. Affects foals 1- 6weeks old - sudden death or acute abdominal pain, depression. Penicillin recommended, but most foals die. Usually PM diagnosis. 

0. Urine leakage from ruptured bladder or rarely from patent urachus or ureters. Common in colt foals. Bladder defect always on dorsal midline - probably a ‘weak point’. Probably ruptures when foal’s abdominal pressure increases during delivery.
   

0. Signs - onset 3-7 days old. Usually only some of urine passes into peritoneal cavity so most foals still urinate externally. Progressive onset of abdominal distension, lethargy, tachypnoea, tachycardia, circulatory failure, mild abdominal pain. Diagnosis made on signs, ultrasonography of abdomen and bladder and peritoneal fluid analysis. 

   Uroperitoneum confirmed by demonstrating ratio of creatinine in peritoneal fluid:serum >2:1 (cannot use ratio for urea since being small molecule equilibrates rapidly across peritoneum). Most foals develop azotaemia, hyperkalaemia, hyponatraemia, hypochloraemia and metabolic acidosis 

Rx - due to metabolic derangements this is a medical and not a surgical emergency - not good surgical candidates until medically stabilised. Attempt to drain abdomen via catheter, although difficult to get large volume off. Administer IV saline to correct Na loss and hyperkalaemia. Correct hypoglycaemia with IV dextrose. Administer antibiotics. Once metabolically stabilised perform surgical bladder closure. 

Perinatal asphyxia syndrome (PAS);

Septic meningoencephalitis

Hypoglycaemia 

Perinatal asphyxia syndrome (PAS); 

Also termed neonatal encephalopathy (NE), hypoxaemic ischaemic encephalomyelopathy (HIE), neonatal maladjustment syndrome (NMS), barker, wanderer and dummy foals.

Exact pathogenesis unclear and likely multifactorial, but involves peripartum cerebral hypoxia/ischaemia. Most foals appear normal for several hours to 1 day, before developing signs of cerebral dysfunction - localised seizures of face and limbs, disorientation, ataxia, loss of righting and suck reflexes, loss of affinity for dam, central blindness, barking vocalisation, loss of thermoregulation, erratic breathing pattern, increasing recumbency, coma and/or general seizures. Secondary FPT, dehydration, hypoglycaemia, metabolic and respiratory acidosis.

No specific diagnostic tests, so diagnose by eliminating other conditions. No specific treatment. Steroids or DMSO often administered but no evidence of efficacy.

Control seizures using diazepam slow IV, detomidine/butorphanol or Na pentobarbitone. Nursing is critical - nutrition, heat, fluids, antibiotics, IgG supplementation, intranasal oxygen etc. Many stabilise by 2-3 days but full recovery takes several weeks. Poor prognosis if not improving within 48h 

Septic meningoencephalitis; 

75% of septic foals show CNS signs including profound depression, coma or seizures, cervical stiffness or pain, hyperaesthesia, weakness or tetraplegia. Confirmed by increased CSF protein and neutrophil count. Rarely culture bacteria from CSF. Treat as for septicaemia. Prognosis - poor 

Hypoglycaemia  

many sick foals are hypoglycaemic, but few are bad enough to develop CNS signs - caused by fasting, stress, hypothermia or sepsis. Best monitor glucose levels of all sick foals so that can treat before clinical signs develop. Signs; weak, lethargy, profound depression, reduced sucking, recumbent, hypothermia, rarely coma/seizures. Treat with 5% or 10% glucose solution IV. 

Umbilicus normally breaks ~5cm from abdomen - dries up <24h. Stump comprises:

•   2 umbilical arteries which connect internal iliac arteries to placenta and which, after birth,

  become round ligaments of bladder

•   1 umbilical vein which connects placenta to hepatic portal vein, which becomes the round

  ligament lying within the falciform ligament after birth

•   urachus - connects foetal bladder to allantoic cavity 

0. Umbilical infections/abscessation; 

0. Infection occurs usually <1week old. Most commonly have infection confined to external umbilicus, with local heat, pain, swelling and commonly no systemic effects. These can be effectively drained and/or treated with systemic antibiotics. More concerning is infection of internal umbilicus – ultrasound useful to detect infection - often have secondary septicaemia. Usually require surgical removal as rarely respond to antibiotics alone. 

0. Patent urachus;  

0. Associated with navel ill, septicaemia, increased abdominal pressure due to straining (eg retained meconium) or prolonged recumbency. Usually occurs soon after when dried umbilical stump drops off. Easily recognized because urine drips from umbilicus and urethra when urinate. Perform ultrasound examination to determine if urachus is infected. Infected urachus requires surgical removal, while uncomplicated patent urachus usually resolve simply with correction of underlying cause eg retained meconium.