Physiological Consequences of Spinal Cord Transection
This section reflects mainly on the physiology of high spinal injury (i.e. something happening in the low C-spine). The reason for this bias in the plethora of interesting physiological effects which are observed, rather than any sort of clinical importance of the injury itself.
The topic of spinal cord injury has been investigated in several SAQs:
- Question 18.3 from the first paper of 2010
- Question 15 from the first paper of 2006
- Question 14 from the first paper of 2005
- Question 2c from the first paper of 2003
- Question 1a from the first paper of 2000
- Question 1b from the first paper of 2000
The canonical resource to answer this question would have to be Chapter 78 from Oh's Manual, Spinal injuries by Sumesh Arora and Oliver J Flower. There, on page 801 an extensive exploration of ICU management is carried out, with all the relevant systems covered.
In brief, one can summarise the effects of spinal cord transection in the form of a table:
Gastrointestinal consequences of spinal injury
Now, in great detail:
Respiratory consequences of high spinal cord transection
With damage to the spinal cord above the T1 level, intercostal and other chest wall muscles become paralysed, with the result that the diaphragm is now solely responsible for the respiratory effort. For a thin strap of muscle, this is a lot of work. Without the chest wall performing its notmal "bucke handle" excusion, the pattern of respiration becomes paradoxical, almost obstructed-looking. The patient gives the impression of breathing with their abdomen: the chest does not rise and fall, but the abdomen seems to heave with each respiratory effort.
The mechanical consequences of this are discussed in a 2007 article by Cardozo, and the lung mechanics of spinal cord injury patients are explored in a 2001 paper by Baydur and Adkins. There are several major issue to consider:
The chest wall no longer assists with lung expansion, and thus the only volume change you can expect is through the displacement of abdominal content by the diaphragm. This diminishes the maximum tidal volume. Similarly, the expiratory effort is an effort of the diaphragm alone; thus the spirometry findings in these people tend to demonstrate a restrictive pattern, with a small volume rapidly exhaled.
the diaphragm cannot generate a sustained effort in situations when tachypnoea is called for, for instance with exertion or in context of metabolic acidosis. The capacity to compensate for acidosis is thus very limited.
The patients seem to breathe easier when supine, particularly if the diaphragm is alone in the generation of respiratory effort. The reaosn for this is thought to be greater stretch of the diaphragm, which places it into a position of increased mechanical advantage.
One might think that respiratory volumes shoudl increase with sitting upright (as is the case for most patients) - but in this case, the gravitational displacement of the abdominal contents plays a detrimental role. The abdominal contents in the quadriplegic patient sloshes around according to the whims of gravity - the abdominal wall muscles are paralysed and atonic, doing little to maintain the position of the abdominal organs. The downward stretch exerted by the displaced abdominal contents may also expand the total intrathoracic volume, but this action places the diaphragm into a position of disadvantage - in this postion, it is already halfway-descended. Thus, the diaphragm has little further travel available, and its contraction only expands the intrathoracic volume by a small proportion. This is a similar problem to the experience of COPD patients, who have a flattened diaphragm.
Much of what happens to the cardiovascular system following spinal cord injury is attributable to two factors: the abolition of descending sympathetic control, and the decreased metabolic requirement of denervated muscle. An excellent article by Teasell et al can be recommended.
The concept of "spinal shock" is discussed elsewhere. However, it is central in the explanation of the cardiovascular consequences of spinal cord injury in the long term. Essentially, the total body sympathetic denervation which occurs with spinal shock is only short-lived. As time progresses, the sympathetic nervous system recovers to some extent- but its recovery is patchy, disorganised and bizarre.
Not only is the vascular smooth muscle tone decreased. The tonic contraction of muscles which is maintained under normal circumstances in the non-paraplegic individual is also lost, and this contributes to the overall decrease in afterload. Blood pressure may fall as a result. This is usually seen in injuries above T6; anything lower than this tends to preserve enough supraspinal sympathetic control to maintain the total peripheral vascular resistance. The reduction in resting systolic blood pressure correlates fairly linearly with the spinal cord level; i.e. the reduction in peripheral vascular resistance is proportional to the number of denervated blood vessels.
There is greater pooling of blood in the maximally dilated venous capacitance vessels, and thus there is diminished venous return to the heart.
The α-adrenoceptors, in the absence of stimulus, become more numerous and thus the peripheral vessels respond more vigorously to infused noradrenaline. These patients tend to require very low doses of noradrenaline if they become septic. The hyperresponsiveness tends to take some weeks to months to develop, and the recently paralyased patient does not tend to exhibit this effect.
Because of the loss of strict sympathetic control, and because of the hyperproliferation of adrenoceptors, the "autonomic" reflex responses in these patients can be wildly exaggerated. For one, any vagal reflex will be amplified because of unopposed vagal action. Additionally, any sympathetic stimulation below the level of transection may lead to a wildly exaggerated reflex sympathetic response, with massive hypertension. Noxious stimuli, bladder distension, constipation, sexual stimualtion - all these can lead to an "autonomic storm".
Obviously with the loss of the efferent limb of the baroreceptor reflex arc, one is unable to compensate for changes in blood pressure with changes in cardiac output. The result is an orthostatic hypotension; it is thought that the main contributor is the decrease in venous return due to pooling of blood in the viscera.
If the spinal cord lesion is in the C-spine, chances are the sympathetic innervation of the heart is lost. The myocardium is thus under unopposed vagal control. The result is bradycardia. Worse yet, manoeuvres which normally result in the simulation of the autonomic nervous system (such as suctioning of the trachea) will have an unopposed vagal response rtaher than a balanced sympathetic-parasympathetic response; the result is a potential for an embarassing vagally mediated asystolic arrest after routine tracheal care.
As a result of abolished sympathetic input, the cardiac output cannot increase in repsonse to stress or exercise. One is unable to compensate correctly for shock states, for anaemia, for any sort of physiological stimulus which would demand increased tissue oxygen delivery. The only way of manipulating cardiac output in these patients (without resorting to inotropes) is the modification of left ventrcular preload, by the increase of LV filling volume. The cardiac contractility should still be subject to normal Frank-Starling relationships.
This topic is explored with exhausting attention to detail in a four-part series, published by Claus-Walker and Halstead in the early 1980s in the Archives of physical medicine and rehabilitation. The references for this can be found below. Instead of dutifully reciting every minor point, I will focus on what is relevant to the intensivist.
The loss of sympathetic innervation, and the ensuing vasodilated state, tends to result in systemic hypotension. Perhaps the efferent arc of the baroreceptor reflex is impaired, but not the afferent arc. The posterior pituitary secretes vasopressin in response to this shock state, and in vast quantities. This causes renal water retention and hyponatremia. As time progresses and normotension is to some extent restored, so does the SIADH resolve - but some hyponatremia may persist, because it seems the spinal injury patients lose their normal diurnal rhytm of vasopressin secretion.
This is related to the exaggerated action of the renin-agiotensin-aldosterone axis. The renal secretion of renin is normally subject to constant descending inhibition by the sympathetic nervous system. When this inhibition is abolished, the juxtaglomerular appartus of the kidney becomes wildly hyperactive, secreting insane amonts of renin into the circulation. The resulting "hyperangiotensinism" is not enough to produce hypertension, but the increase in aldosterone secretion is certainly enough to cause features of hyperaldosteronism in some individuals. Hypokalemia and hypernatremia may be produced as a consequence.
The combination of inactivity and muscle wasting leads to adiposity, and to insulin resistance. Almost half of spinal injury patients become type II diabetics as a consequence. Spinal cord injury thus results in increased postprandial insulin levels, and this increase is sustained for longer than it would be in intact patients, resulting in a "reacive hypoglycaemia" some hours after a meal.
This will not be noticed until it is very late, as the normal sympathetic response to hypoglycaemia is abolished. The normal response would be a sympathetic-driven increase in muscle gluconeogenesis, and decreased glucose uptake by the muscle tissue. In quadriplegic patients, this will not happen, and the high insulin levels will be unopposed. A way of managing this might be the reduction of carbohydrate intake, avoiding large carbohydrate-rich meals.
As the muscultaure fo the body is denervated, the muscles - bereft of central neural tone, and starving for it - begin to reflexively sprout massive amounts of acetycholine receptors. These receptors are extruded onto cell membranes all over the place. They are just waiting for acetylcholine, or its equivalent. Imagine, as suxamethonium comes along and locks these channels open. Cations stream in both directions. The serum potassium rises precipitously. Cardiac arrest ensues, typically about 4 minutes after induction (just when you were about to sit down).
How high does the potassium go? The first such complications were noted in a 1970 article by Tobey et al. I don't have access to the full paper, but from what I can see in the preview, the authors reported on 4 cases of cardiac arrest, in which the serum potassium levels were taken every couple of minutes after the administration of suxamethonium. I note the especially unlucky Patient Number Four, whose potassium rose from 3.5 to about 14.0mmol/L.
Fortunately, this effect is short-lived even without antihyperkalemic therapy, and the potassum dutifully returns into the intracellular compartment within 20 or so minutes. Subsequent authors have used this as a cautionary tale, to steer people away from using depolarising NMJ blockers in spinal cord injury patients.
Early on, people recognised that "recumbency" is an important factor in the genesis of urinary tract calculi. Disuse of bone results in bone wasting, and associated elevated alkaline phosphatase levels. The precise mechanisms for this are incompletely understood. Is it merely the loss of mechanical loading? Are pathyroid glands somehow involved? Parathyroid levels frequently remain normal in the face of extreme bone wasting. As bone is demineralised, serum calcium and phosphate levels increase, resulting in hypercalciuria and renal calculus formation. Huge lacerating calculi can form without being noticed by the denervated ureters, and presentation is typically delayed until the patient notices that they are passing frank hematuria through their IDC.
To put correctly, the spinal injury patient develops "poikilothermia", which is the deregulation of body temperature control leading to abnormally raised core temperature in hot environments, and abnormally low temperature in cold environments. The main reason for this is the loss of sympathetic control. Consider how much of one's thermoregulatory function is the result of piloerection, sweating, and vasodilation or vasoconstriction. Without these mechanisms, one is unable to control how much of one's body heat one exchanges with the external environment. Robbed of such reflexes, the tetraplegic is limited to altering their thyroid hormone secretion as a means of temeperature regulation - which is obviously useless in the context of rapid changes.
According to a 1981 evaluation of 567 spinal injury cases, during the first month post injury, these complications consisted of ileus, gastric dilatation, the body cast syndrome, peptic ulcer disease, and pancreatitis. A more recent review article elaborates extensively on this topic.
The severity of this seems to correlate with ascending level of spinal cord injury. Gastric emptying is impaired because of a loss of sympathetic control of autonomic reflexes. The normal response to oeseophageal distension is gastric relaxation (to receive food); however in the spinal trauma animal models this vagal reflex arc somehow becomes hyperactive, and leads to over-relaxation of the stomach. The lazy stomach refuses to proceed with normal peristalsis, and becomes filled with food material. The incidence of this is reported as 10%, at least for gastric dilatation of any clinical significance. The implications are serious - a dilated stomach and a lax lower oesophageal sphincter are a recipe for aspiration.
The pooling of blood in the lower body tends to lead to intenstinal oedema, and thus makes the bowel heavier, with more resistance to normal peristalsis. However, this is not the whole picture. Control of evacuation is also lost, and no spinal cord–mediated peristalsis occurs, resulting in slow stool propulsion. Left to control the bowel all on its own, the myoenteric nervous system becomes disorganised, and this results in ileus early in the history of a spinal cord injury.
This is the syndrome of acute gastric dilatation associated with the application of a full-body plaster cast, which is thankfully no longer practiced. One article from 1970 recalls a particularly high mortality rate from this syndrome, due to "pernicious vomiting" and aspiration. The mechanism of this syndrome is the obstruction of the duodenum by the superior mesenteric artery, which occurs when the normal fatty jacket is shed from the mesenteric root. Thus unprotected, the duodenum becomes squished between the superior mesenteric artery and the aorta - both fairly robust structures. The feeble duodenum is unable to squeeze food boluses past such an obstruction, and gastric dilatation is the result.
This seems to be a common complication early in the progress of this disease. Again, dysautonomia is probably to blame - particularly the unopposed vagal influence on the stomach, resulting in a forceful muscarinic stimulus of the parietal cells, which dutifulyl pump out vast amounts of hydrochloric acid.
In general, it seems to greatest risk of gastric ulceration is between the fourth and tenth day after the spinal injury. It seems later in the course of chronic spinal injury the lifetime risk of death from peptic ulcer perforation reverts to the normal population average.