The Septic Patient. Sam McMillan VTS (Anaesthesia) DipAVN (Medical) RVN

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1 The Septic Patient Sam McMillan VTS (Anaesthesia) DipAVN (Medical) RVN Sepsis, severe sepsis and septic shock are common causes of morbidity and mortality in our veterinary patients. It is important that as nurses we can recognise that a patient may be becoming septic and know when a septic patient shows deterioration in clinical signs. Although very rewarding to nurse in an intensive care r high dependency setting these patients require early and aggressive intervention and first class, dedicated nursing care and supportive therapy if they are going to stand any chance of recovery. Systemic Inflammatory Response Syndrome (SIRS) This syndrome refers to the clinical signs of systemic inflammation. This may be due to infectious causes or non-infectious causes such as trauma, heat stroke, pancreatitis, burns and neoplasia. The systemic response occurs when localised inflammatory response becomes out of control and affects tissues remote to the original site of localised inflammation. The inflammatory mediators responsible for the systemic response are the same as the mediators that elicit the local inflammatory response: Leucocyte and endothelial activation Cytokines Arachodonic acid metabolites (prostaglandins, leukotrines) Reactive oxygen metabolites Activated coagulation and platelet cascades Complement activation Once activated these cascades exert positive feedback which ensure continuation of the inflammatory cascade causing increasing systemic effects. SIRS can be thought of as an imbalance between pro-inflammatory and antiinflammatory cascades.

2 SIRS is classically represented by the patient as two or more of the following: Tachycardia >120bpm in dogs and >225bpm in cats Bradycardia (cats) <140bpm in cats Tachypnoea or hypocarbia > 20bpm in dogs or PaCO2 <32mmHg and > 40bpm in cats Hyperthermia >39.7 C Hypothermia < 37.8 C in dogs and <37 C in cats Leucoocytosis >18000x10 9 /L in dogs >19000 x10 9 /L in cats Leucopaenia <5000 x10 9 /L or > 10% bands Other clinical manifestations that may be seen with SIRS are: Mild to moderate depression Poor appetite Hyperglycaemia Vasodilation red MM, accelerated CRT (< 1 sec) Bounding pulses Normal to low CO Normal to low arterial and central venous pressure Diarrhoea Heart murmur Normal to hyperactive coagulation Normal to mildly impaired liver function Non specific increase of liver enzymes Hypoalbuminaemia Sepsis The clinical syndrome caused by infection of the patient by micro organisms and the patient s inflammatory response to it. Micro organisms may be bacterial, viral, protozoal or fungal. Sepsis is basically SIRS with the proven evidence of infection. The main cause of sepsis in dogs and cats is septic peritonitis. The most common cause of septic peritonitis is leakage of gastro-intestinal (GI) contents secondary to foreign bodies, neoplasia, dehiscence of surgical biopsies and enterectomies, ulcers etc. Other less common causes of septic peritonitis are abscessation, contamination from the bladder, uterine rupture and GI disease such as salmonella infection.

3 Other causes of sepsis in the dog and cat include pneumonia, pyelonephritis, trauma, pyothorax, bite wounds, osteomyelitis, septic arthritis, deep pyoderma, parvovirus and bacterial endocarditis. Questions to ask in triage Has there been recent traumatic injury? Is the patient diabetic? Has the patient had a dental recently/ have the owners recently started cleaning the patient s teeth? When was the patient last in season if female and entire? Is there a history of diarrhoea, vomiting, weight loss? Is the patent a scavenger? Is this a working dog? What drugs is the patient currently receiving? What exposure to other animals and wildlife does the patient have? Is the patient immunosuppressed? Clinical Signs of Sepsis Pyrexia Hypothermia (especially cats) Brick red mucous membranes with CRT < 1 sec as the syndrome progresses mm may be cyanotic, dusty pink, grey or pale with prolonged > 2 sec CRT. Tachycardia Bradycardia (especially cats) Tachypnoea Altered mentation Bounding pulses initially then weak pulses in later stages Icterus may be present due to cholestatis, haemolysis of red cells, hepatobillary pathology or underlying liver disease Other parameters indicating sepsis may include: Leucocytosis Leucopaenia Normal WBC count >10% neutrophils Arterial hypotension Arterial hypoxaemia

4 Acute oliguria Increased creatinine Hyper or hypo coagulobility Thrombocytopaenia Hypoglycaemia Hyperbilirubinaemia Tissue perfusion parameters e.g. hyperlactataemia Severe Sepsis This is defined as sepsis progressing to the multiple organ dysfunction syndrome (MODS). Septic Shock Septic shock is a form of distributive shock. Patients with clinical signs of infection and signs of shock are by definition in septic shock. This is the syndrome of sepsis associated acute circulatory failure. This is accompanied by persistent arterial hypotension, despite efforts to provide volume resuscitation, together with perfusion abnormalities e.g. lactic acidosis and oliguria. Disseminated Intravascular Coagulation (DIC) Any disorder which causes a widespread activation of the coagulation cascade can cause DIC. The most common cause is SIRS. DIC begins as a hypercoagulable, thrombotic state associated with microvascular thrombi. Microthrombi can lead to ischeamia and damage to major body systems. Fibrinolysis leads to an increase in fibrin degradation products (FDPs) which inhibit thrombin activity. A later hypocoagulative state is created by a depletion in platelets and consumption of clotting factors and the increase in FDPs. Clinical signs in his phase may include: Petechiae Ecchymoses Epistaxis Prolonged bleeding from venepuncture sites GI haemorrhage Haematoma formation Blood results in the patient with DIC may reveal:

5 Prolonged prothrombin time (PT) Prolonged activated partial thromboplastin time (PTT) Thrombocytopaenia Increased or decreased blood fibrinogen levels Low antithrombin levels Positive FDPs or D-dimers (specific FDPs) Treatment for DIC Correct the underlying cause. Maintain adequate tissue perfusion i.e. fluid therapy Prevent/ control acid base disturbances Fresh frozen plasma (FFP) may be beneficial to patients exhibiting signs of haemorrhagic coagulopathy but for those patients without bleeding tendencies FFP has not been shown to improve outcome. Multiple Oran Dysfunction Syndrome (MODS) When inflammation becomes systemic, organs, tissues and systems remote from the site of original insult can become damaged. Organs commonly involved include the lungs, kidneys, vascular endothelium, heart, liver and clotting system. The amount of organs or systems affected is inversely proportional to survival in critically ill patients. Clinical manifestations of MODS may include some of the following: Moderate to severe depression No appetite Sub-normal core temperature Hypoglycaemia Leucopaenia or a large, rapid decrease in leucocyte count with a marked left shift and toxic neutrophils Vasoconstriction Low CO Low arterial and central venous pressure Tachycardia, tachypnoea, hyperventilation High venous oxygen, reduced arterial-venous oxygen difference Heart murmur Haemorrhagic diarrhoea Hypoactive coagulation - petechiation, echimosis Lactic/metabolic acidosis

6 Moderate to severe impairment of organ function Moderate increases in liver enzymes Hypoalbuminaemia Acute Respiratory Distress Syndrome (ARDS) Acute lung injury (ALI) is the clinical state of impaired gaseous exchange caused by acute injury to the lining of the alveoli. Damage is caused by inflammatory mediators producing inflammation, cellular infiltration and subsequent capillary leak. This capillary leak results in fluid accumulation in the alveoli. Damage is due to a catrastrophic event which can either be pulmonary e.g. aspiration pneumonia, pulmonary contusion, smoke inhalation, noncardiogenic pulmonary oedema or extrapulmonary (systemic) e.g. sepsis and/or SIRS in origin. ALI in critically ill patients is often a manifestation of SIRS affecting the local pulmonary system. Acute respiratory distress syndrome (ARDS) is simply a severe form of ALI. ARDS-ALI can be further defined by a low oxygenation ratio e.g. PaO 2 to FiO 2 ratio. Patients with ALI have an oxygenation index of less than 300 whereas ARDS is defined by an oxygenation index of less than 200. Remember normal lungs have an oxygenation index of approximately 500. Recovery from this type of lung injury can take weeks and the supportive treatment for ALI and ARDS is often mechanical ventilation. Less severely affected patients should be supported with cage rest and supplemental oxygen. Nursing Care Wear gloves maintain aseptic techniques, these patients are immunocompromised. Oxygen supplementation keep the SpO 2 over 93% Obtain I/V access more than one, jugular vs. peripheral? Monitor and record all vital signs Monitor pulse profile Auscultate thorax- assess heart for abnormal rate/ rhythm, muffled heart sounds, assess lung sounds for crackles and wheezes. Obtain blood samples for PCV, TS, BG, BUN, creatinine, ACT, APTT/PT, haematology and biochemistry, electrolytes, blood gases, lactate Fluid therapy crystalloids, colloids, blood component therapy

7 ECG Monitor BP +/- CVP Assist with diagnostic imaging Administer and monitor drugs inotropes, vasopressors, antibiotics, gastric protectants, antiemetics, anti-thrombotics Analgesia and pain assessment Auscultate thorax- assess heart for abnormal rate/ rhythm, muffled heart sounds, assess lung sounds for crackles and wheezes. Monitor urine output General nursing care e.g. turning etc. TLC, mental stimulation The goals of our supportive therapy are to restore CO and tissue perfusion, to increase oxygen delivery, to maintain systemic blood pressure in vital circulation and to limit excessive vasoconstriction or vasodilation. If any parameters are indicative that supportive therapy is not improving the patient s clinical picture or if clinical signs are actively deteriorating the veterinary surgeon should be notified immediately. References and Further Reading Lesley G. King and Amanda Boag BSAVA Manual of Canine and Feline Emergency and Critical Care, 2d ed. Gloucester: BSAVA. Wayne E. Wingfield and Marc R. Raffe The Veterinary ICU Book. Wyoming: Teton New Media Karol A. Matthews Veterinary Emergency and Critical Care Manual, 2d ed. Ontario: Lifelearn. Douglass K. Macintire et al Manual of Small Animal Emergency and Critical Care Medicine. Philadelphia: Lippincott Williams & Wilkins. Deborah C. Silverstein and Kate Hopper Small Animal Critical Care Medicine. Missouri: Saunders Elsevier.