There is no doubt that tick paralysis is a condition designed to test us. The disease is very common across the Australian eastern seaboard. Although seasonal, isolated cases turn up year round when you are least expecting them. The condition can be easy to misdiagnose in the early stages, then frustrating to treat if a patient is severely affected. When tick paralysis patients decompensate, it is usually associated with respiratory failure.
This may be caused by severe musculoskeletal paralysis, upper airway obstruction, pulmonary parenchymal disease or a combination of both. Early recognition of respiratory failure and differentiation of the cause should help us treat patients severely affected by tick paralysis. Veterinarians become very good at assessing and monitoring a patients respiratory function. Examining the patient allows us to determine respiratory rate and, effort. Auscultation can detect adventitial lung sounds: wheezes, crackles, and stridor. We can then assess whether the patient has enough respiratory drive or alternately is “simply working too hard”. The patients which work too hard to breathe become exhausted – this breathing pattern is NOT sustainable!
We have seen many patients with oxygen saturation of >95% but with a steadily climbing CO2. A venous blood gas is adequate for measuring CO2 levels. If PvCO2 (or PaCO2) is greater than 60mmHg, the patient is severely hypoventilating. This could be due to upper airway obstruction or neuromuscular failure. Profound hypercapnoea is associated with respiratory acidosis, hypotension, poor myocardial function and central depression. Although we certainly have had patients survive with a PaCO2 of much greater than 60, this should be ringing alarm bells and raising the possibility of upgrading the respiratory support. Either alleviate the upper airway obstruction (intubate) or institute IPPV
Blood gas analysis can give a more complete assessment of respiratory function. Most cartridges give additional information about electrolytes and acid base balance, which can really help tailor the fluid therapy plan. Complete clinical assessment of a patient with severe tick paralysis should involve careful physical examination, pulse oximetry, chest radiographs and blood gas analysis.
An arterial blood gas analysis provides an accurate measurement of oxygenation, which unlike pulse oximetry is not affected by perfusion, mucous membrane pigment or patient movement. A patient with a PaO2 of < 60 mmHg is severely hypoxaemic and needs oxygen therapy. If the severe hypoxaemia is not resolved with oxygen therapy mechanical ventilation is required.
Blood gas equipment can be used to monitor electrolyte levels, blood lactate and acid base balance in addition to pulmonary function. This can help plan a critical patients’ fluid therapy and has application to managing many severe illnesses including DKA, HGE, and Addison’s disease.
When do I perform a coagulation study?
I perform a coagulation study in any patient suspected of having a “bleeding disorder”. The most common patients would be patients suspected of having rodenticide toxicity. Dogs with rodenticide toxicity may have marked elevations in PT and APTT. Because the Vitamin K dependant clotting factors have the shortest half life, the PT will typically be elevated first. With time, both PT & APTT are elevated. Some dogs with rodenticide toxicity will also be thrombocytopaenic. Testing coagulation status is also useful for supporting the diagnosis and helping to differentiate snake envenomations. Dogs with brown, tiger, black, taipan and mulga snake envenomations may be coagulopathic. Black snake or red belly black snakes have a haemolytic toxin and tiger, black, taipan, mulga snakes and small eyed snakes possess a myotoxin resulting in elevations in CPK in the 10s to 100s of thousands IU.