In this case study, a 9-year-old intact male miniature donkey was referred to Davis veterinary teaching hospital’s large animal emergency services for evaluation of colic of approximately 24 hrs duration. The patient is individually housed on irrigated pasture with an adjacent mature oleander hedge. Concerning the onset clinical presentation, a tentative diagnosis of oleander toxicosis was made based on the proximity of the mature oleander hedge.
Oleander is an ornamental evergreen shrub that is commonly found in the southern united stated and California.
Oleander (Nerium oleander) contains more than 30 different cardiac glycosides of the class cardenolides with oleandrin being most important. Oleandrin may affect the cardiovascular, nervous and gastrointestinal systems. Oleander is unpalatable to animals but may still be ingested in some situations .
Oleandrin binds to extracellular binding sites inhibiting Na+K+ ATPase pumps which results in a cascade of the effects resulting in cardiac arrhythmia. This appraisal will discuss the mechanism behind cardiac arrhythmia and also the increase in central venous pressure resulting in pulmonary oedema.
Cardiac muscles form a functional syncytium allowing action potential to propagate throughout the heart. Pacemaker cells are cardiac cells that are located in the sinoatrial node (SA node) located in the right atrial wall that depolarise towards threshold spontaneously. Due to the presence of pacemaker cells, the heart does not need nervous innervations to beat but motor-neuron (sympathetic and parasympathetic) does affect the heart rate by influencing the rapidity of pacemaker cells to depolarises to threshold.
Each heartbeat is initiated by an action potential that arises spontaneously in pacemaker cells of the SA node.
This action potential propagated toward the atrioventricular node (AV node) then to the ventricles via the bundle of His. Cardiac muscle fibers have a very long action potential duration. On top of that, calcium channels are also present in the cardiac cell membrane. Ca2+ has an extremely important role in prolonging cardiac action potential allowimg a maximum ventricular filling before ventricular systole.
Equids have their atria and ventricles electrically separated from each other by non-conducting fibrous tissues except at the AV node. This results in a delay in conduction between the atrial and ventricular depolarization allowing ventricular filling before ventricle systole. Normal equids have a high parasympathetic tone that may delay or block AV nodal conduction. Conduction delay may be measured by PR interval.
Very often, horses are presented with cardiac arrhythmia but are usually associated with high vagal tone originating from the SA or AV node. This happens commonly during rest or a change from sympathetic to parasympathetic predominance. These are often known as physiological arrhythmia.
There is also pathological arrhythmia as in this case, the donkey was presented with suspected ventricular tachyarrhythmia. The normal heart rate of donkeys is between 36-68bpm and the donkey presented was at 120bpm indicating tachyarrhythmia. Ventricular arrhythmia originated from the ventricular myocardium has many underlying causes but in this case, the presence of oleandrin. Impulses are conducted through the ventricles differently and are dependent on cell to cell conduction. The resulting QRS complex will have a different morphology and longer duration. Ventricular tachyarrhythmia shows wide QRS-complexes with partially hidden P-waves not associated with QRS-complexes termed atrioventricular dissociation.
The main active agent of concern in oleander is oleandrin. It has been observed that oleandrin causes high calcium concentrations in cardiomyocytes which results in the inability to release accumulated calcium.
Calcium release channels in ryanodine receptors are blocked, interfering with calcium uptake through inhibition of K+Na+ ATPase disrupting function of calcium release in sarcolemma. Oleandrin exerts its effects by binding with an extracellular portion of the pump inducing a conformation change in the enzyme by stabilizing it in the transition state which decreases the active transport of sodium with consequent potassium excretion. Increasing intracellular sodium levels inhibits Na+Ca2+ exchanger (NCX) resulting in increasing intracellular Ca2+ levels responsible for the positive inotropic effect and toxicity.
Cardenolides may also inhibit efflux of calcium from cells resulting in a further increase in intracellular calcium concentration. This overall increase in calcium raises the resting membrane potential leading to an increased rate of spontaneous cell depolarization.
Inhibition of K+Na+ ATPase results in cellular calcium overboard and a delay post-depolarisation developing abnormalities in electrical conductivity of the myocardium, arrhythmia, and loss of myocardial contractibility. The sympathetic outflow also increases which sensitizes the myocardium exaggerating all toxic effects causing a reduction in normal electrical conductivity of myocardium. These effects are however reversible. The lethal dose of oleander is as low as 0.005% of the animal’s body weight in dry leaves and symptoms surface at 30mins to a few hours post-ingestion. Commonly reported signs include sinus bradycardia, AV block, atrial or ventricular fibrillation and asystole.
Oleander toxicoses are usually diagnosed at post mortem. Other common ways of documenting oleander toxicoses includes thin layer chromatography of ingesta, faeces or urine. Serum digoxin may also be used as oleandrin and its metabolite oleandrigenin have high cross-reactivity with some digoxin and digitoxin immunoassays.
In an attempt to treat the tachyarrhythmia, lidocaine and phenytoin are used. Both lidocaine and phenytoin are class 1B antiarrhythmic drugs that bind to and block fast sodium channels that are responsible for rapid depolarisation. This results in decreased conduction velocity in non-nodal tissues reducing the rate and magnitude of depolarisation.
The slope at phase 0 is dependent on fast sodium channels. By blocking it, the amplitude of slope at phase 0 is reduced thus reducing action potential. This drug does not affect nodal tissues as the action potential of nodal tissues is carried by calcium. If a cardiac cell depolarises rapidly, the adjacent cell will also rapidly depolarise resulting in a faster regeneration and transmission of action potential between cells. Therefore tachycardia resulted from abnormal conduction may be suppressed by blocking sodium channels.
Class 1B antiarrhythmic drugs also reduced the effective refractory period. The effects of a reduced effective refractory period do not relate to sodium channel blockage but potassium channels that are involved in repolarisation of the action potential in phase 3. These channels regulated potassium efflux from the cell thus regulating repolarisation.
In normal breathing, diaphragm and intercostal muscles contract increasing the volume of the thoracic cavity creating a negative pressure relative to the atmospheric pressure. Air enters the lungs and gas exchange occurs between capillaries of pulmonary vasculature and alveoli via diffusion.capillaries have clefts and pores between endothelial cells that allow water and solutes to move across them. Blood content creates an osmotic pressure that draws water in from the interstitial spaces. In homeostasis, the control of fluid is due to the balance in hydrostatic pressure in capillaries. This encourages fluid to leave the intravascular space and blood oncotic pressure draws the fluid back in. Excess fluids are drained from the interstitial spaces via lymphatic vessels.
Increased capillary hydrostatic pressure favors a greater filtration of water. This may result from an increase in arterial blood pressure, a decrease in arteriolar resistance or increase backing up of venous blood that is likely in this case study. The increase in central venous pressure cause blood to accumulate in systemic capillaries raising capillary hydrostatic pressure facilitating water filtration and the likelihood of developing oedema.
Marked systemic oedema and ascites are common in patients with right ventricular heart failure and in contrast, pulmonary oedema is often caused by left ventricular heart failure. In this case study, an ultrasound revealed pleural effusion and fluid was removed percutaneously in thorax suggested that both ventricles might be affected. This suspicion is also consistent in the monomorphic ventricular tachyarrhythmia reflected in the ECG.
Pulmonary oedema is a result of excessive filtration of fluid making it hard to breathe. The most common cause of pulmonary oedema is increased capillary pressure. By increasing pulmonary venous pressure, capillary pressure increases and this is commonly caused by left ventricular or mitral valve failure. The inability of the heart to pump sufficient blood around the body cause blood to back up in the pulmonary vasculature leading to an increase in pulmonary capillary pressure. In response, the body naturally vasoconstricts due to the presence of metabolites exacerbating the already build up in pressure in the pulmonary capillaries. In the discussed case, there were signs of increased heart rate (tachyarrhythmia), pleural and mild pericardial effusion. These signs suggested a net filtration of fluids from the capillary beds.
Clinical presentation of pulmonary oedema often characterized by the onset of dyspnoea associated with the rapid accumulation of fluid within the lungs as a result of elevated cardiac filling pressure. In severe cases, the excess fluid forms froth in the lungs obstructing airways. Pulmonary oedema that is a direct result of cardiac problem are called cardiogenic pulmonary oedema (CPO). Causes of CPO that’s is most likely associated with the discussed case could be the tachyarrhythmia associated increase in central venous pressure.
Pulmonary oedema can be corrected by percutaneous removal of accumulating fluid which is done in this case resolving the tachypnoea and respiratory stridor. Oedema can also be corrected with the use of diuretics that’s is also administered in this case study.
Diuretics drugs promote diuresis by altering sodium handling of the kidneys, if the kidneys excrete more sodium, water excretion increases. This is achieved by inhibiting the reabsorption of sodium at various segments of the renal tubular system by blocking multiple nephron sites.
The drug given to the donkey is furosemide which is a loop diuretic. The loop diuretic works in an all-or-none fashion and must be filtered at the glomerulus reaching a therapeutic concentration at the site of action.They are short-acting drugs. Loop diuretic inhibits Na-K-Cl cotransporter (NKCC) in the thick ascending limb that reabsorbs about 25% of sodium load, therefore, inhibiting this cotransporter results in a significant increase in the distal tubular concentration of sodium reducing hypertonicity of surrounding interstitial. This increases urine production by reducing water absorption at the collecting duct resulting in diuresis and natriuresis. Because it acts on the thick ascending limb which handles a significant fraction of sodium reabsorption, it is a very powerful diuretics.
Diuretics also decrease blood volume and therefore venous pressure. The decrease in venous and capillary hydrostatic pressure reduce filtration rate and promote capillary reabsorption and therefore resolving pulmonary oedema presented in this case.
This donkey survived oleander toxicity through the use of supportive care and the use of antiarrhythmic drugs.
The main problem presented in this case is the ingestion of oleander by a donkey leading to the clinical signs that revolved around the cardiovascular and pulmonary system. Oleander contains oleandrin that is a cardio glycoside that impacts the gastrointestinal, nervous and cardiovascular system.
Problems with the affected cardiovascular system often characterized by arrhythmia, tachyarrhythmia in this case. This problem is address by the use of antiarrhythmic drugs that are fast Na+ channel blockers decreasing effective refractory period. Changes in the cardiovascular system result in the change in venous pressures resulting in net filtration of fluid in the body causing oedema. Oedema is often treated by loop diuretic, furosemide in this case and they act on NKCC channels of the thick ascending limb of the nephron. Although loop diuretics are a strong diuretic agent, there are side effects not discussed in the appraisal that has to be considered on a case to case basis.
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