Sepsis – Ripley

Ripley was a 12 hour filly foal presented to the Camden Equine Centre because she was unable to stand and suckle after birth. Ripley was born under a “red bag” delivery. Although the red bag was cut and the foal rescued immediately, she was unable to stand and nurse normally like other foals.

Ripley recumbent at presentation

The filly was supported at the farm initially with antibiotics and round the clock nursing care. A stomach tube was placed and the filly was tube fed with the mare’s colostrum initially, and subsequently mare’s milk every 2 hours to maintain energy and hydration. The filly was also administered a commercially produced equine plasma to provide immunoglobulins. As the filly did not show much improvement overnight, she was brought into the Camden Equine Centre’s Neonatal ICU where she was managed by equine medicine resident Dr Celine Lee, a team of dedicated interns and residents under the supervision of equine medicine specialist Dr Liz Tee.

Ripley was in a comatosed condition when she arrived at the Camden Equine Centre NICU. She had no suckling reflex at presentation. Other abnormalities noted at physical examination include increased redness of her sclera and coronary band. Our immediate concern for the filly was the “red bag” delivery and consequences of this abnormal birthing event, namely lack of oxygenation to the brain due to suffocation from the “red bag”. Asphyxia to the brain leads to a syndrome called Hypoxic Ischemic Encephalopathy (“dummy foal” syndrome). Increased redness of sclera and coronary band are strong suggestions of sepsis (infection of blood).

Laboratory investigation of the filly included serial arterial blood gas analysis, full blood analysis, blood culture and serum IgG levels. Her initial arterial blood gas showed reduced oxygenation and a moderate increase in blood lactate levels. Initial hematology revealed a significant reduction

Ripley’s hyperaemia of conjunctiva

in white blood cell levels, supporting the initial suspicion of sepsis. Other diagnostic tests performed included thoracic, abdominal and umbilical ultrasound.

Emergency treatment of the filly included commencement of intravenous fluid therapy, intranasal insufflation with oxygen, intravenous plasma administration, systemic antibiotics to combat sepsis, judicious use of systemic antiinflammatories, enteral feeding via stomach tube with mare’s milk, neuroprotectants and required nursing care round the clock.

Ripley remained mostly recumbent during the first 4 days of hospitalisation with marginal improvement in her demeanour and neurological function. She encountered several complications during her hospitalisation. The first complication was a rapid drop in blood pressure and oxygenating capacity to her organs due to sepsis. During severe sepsis, the body produces inflammatory cytokines to combat the infection. These inflammatory cytokines, when produced in large numbers, can cause deleterious effects to the host body, including depression of blood pressure, dysfunction of multiple organs and eventually death.

Resuscitation efforts included increasing volume of IV fluids to increase intravascular volume and addition of vasoactive agents to improve systemic blood pressure. The filly responded eventually to a combination of 2 vasoactive agents (include picture of dobutamine and noradrenaline in new fluid pump).

On day 5 of hospitalisation,  there was a sudden and noticable increase in respiration effort and generalised muscle fasciculation. A repeat blood gas analysis revealed an unexplained metabolic alkalosis and a severe reduction in blood potassium level. We suspected that her muscle weakness was due to this severe reduction in blood potassium level.

Resuscitative measures for this  additional complication included intravenous supplementation of potassium, magnesium and intensive monitoring of her blood potassium level. The filly’s blood potassium levels were slow to improve but eventually normalised after 2 days of therapy.

Ripley subsequently showed clinical improvement with regards to her mentation and strength. She was showing more interest in her surroundings and exhibited “teat seeking” behaviour. She was initially only able to rise with some assistance and only able to stand for less than a minute at a time. By day 11 of hospitalisation, the filly grew strong enough to rise unassisted and successfully latched on the mare’s teat to nurse normally.

Ripley was discharged after 2 weeks of intensive care. She is currently growing fast and strong and happy socialising with other herd mates.


Sepsis can be defined as presence of both infection within a host, and the systemic response of the host towards the infection. It is the most common cause of foal death during the neonatal period, and often develops together with other neonatal diseases such as hypoxic ischemic encephalopathy or prematurity, increasing the complication, length and cost of treatment.

Ripley and mummy at home

Foals can become septic in utero, or be infected after birth. Common portals for infection include gastrointestinal tract and the umbilicus. Foals are essentially immune naïve at birth, that is they do not know how to mount an immune response to infections, hence making them extremely vulnerable to sepsis especially within the first 7 days of life. Foals require immunoglobulins from the mare’s colostrum, hence it is vital that the mare has good quality colostrum, and the foal ingest the colostrum within the first hour of life.

In severe sepsis, septic shock can occur. Patients with septic shock are considered extremely critical and can often lead to death from multiorgan failure. Cornerstone for treatment of sepsis remains infection control, cardiovascular support, respiratory support and nutritional support.