The Vitals: Dysautonomia

by
|
Reading Time: 4 minutes
Picture of Obiajulu Anozie
Obiajulu Anozie
Critical Care Physician trained at Cooper University Hospital. Special interests include: Physiology, Ultrasonography, Echocardiography....and Video Games.

The Pre-brief

Consider the following two scenarios:

  1. 61 y/o male diagnosed with Guillain-Barré Syndrome is admitted to the ICU and intubated. The following day his temperature is elevated at 104 °C and the patient is started on a cooling blanket. Shortly afterwards, his blood pressure reads 221/104 and labetalol IV push is administered. His blood pressure plummets to 60/39 prompting a fluid challenge and IV vasopressors.
  2. 73 y/o female presents shortly after cardiac arrest. She completes therapeutic hypothermia but remains unresponsive. The Respiratory Therapist performs routine tracheal suctioning and her heart rate progressively slows until asystole is shown on the monitor. Code Blue is immediately called overhead.

The above represent major physiological disturbances caused by the autonomic dysregulation of our most vital organs and their key functions. When this occurs, it is called “Dysautonomia”: a diagnosis frequently observed in many ICU’s today, and one which may confer significant morbidity and mortality if not carefully addressed. The following is a brief review of the autonomic nervous system and addresses examples of some commonly observed phenomena when Dysautonomia is present.

The autonomic nervous system (ANS), a division of the peripheral nervous system (PNS), functions to interpret data about the body’s constantly fluctuating internal/external environments and use this information to modulate the activity of our vital organs such as heart, lungs, blood vessels etc. In order to accomplish this, the ANS utilizes a highly sophisticated network of sensory input and motor outputs that function to process data and, in turn, deliver a swift yet appropriate response. The key here is to maintain homeostasis among all the body’s vital organs and balance the sympathetic and parasympathetic outflow that each of them receive.  See diagram below for examples!

In the critical care setting, it is not uncommon to encounter patients who have sustained an insult that disrupts the ability of the ANS to maintain this balance. This may result in some serious, potentially life-threatening physiological derangements to vital organ function. Insults may occur in a variety of ways and may affect the ANS at multiple sites including the inhibitory brain centers in the hypothalamus, the descending inhibitory pathways from the brainstem and the spinal reflex arcs among others. Some notable causes of this disorder are listed in the table below:

Dysregulation of the ANS, or Dysautonomia, results in imbalances between sympathetic and parasympathetic outflow to target organs. Based on the affected organ/organs, clinical symptoms may manifest as paroxysmal episodes of sympathetic or parasympathetic hyperactivity or even as hyper-exaggerated responses to normal stimuli.

Treating this condition can be tricky.  Life-threatening fluctuations in vital parameters such as heart rate and blood pressure demand immediate attention; however, in some occasions, treatment leads to hyper-exaggerated responses that are similarly life-threatening. In Guillain-Barré Syndrome, for example, drug sensitivity may be so heightened that treating dangerously high blood pressures may result in dangerously low ones. Through primarily retrospective studies, there is emerging data suggesting the use of opioids such as morphine and fentanyl as an effective strategy.  Opioids have proven effective at controlling blood pressure with the added safety benefit of less risk of hypotension. If additional control is needed or opioids prove ineffective, intravenous antihypertensives such as labetalol and nicardipine are likely a better choice, over long-acting oral agents, due to their short-acting effects which can be quickly titrated. Continuous blood pressure monitoring via an arterial line may be useful particularly in highly labile patients and especially if there is consideration towards starting an oral agent.

Mechanically ventilated patients also need to be monitored for sudden, paroxysmal episodes of hypotension and orthostasis. This is typically the result of uncontrolled parasympathetic and vagal hyperactivity. Potentially useful strategies include avoiding prolonged periods in the supine position along with compression stockings. In refractory cases, oral alpha-agonists (e.g. midodrine) or fludrocortisone can be effective. Patients should also be monitored for paroxysmal episodes of bradycardia caused by vagal hyperactivity. Paroxysmal bradycardia may be mild; however, patients may even occasionally experience brief periods of asystole during common patient maintenance activities such as tracheal suctioning! Consideration for pacemaker placement, either transvenous or permanent, may be the optimal strategy in such scenarios.  If sinus tachycardia is observed, first consider whether it is being caused by an acute physiological disturbance such as pain, hypovolemia, fever, or infection before initiating beta blockers. To avoid unnecessary and repetitive blood cultures it should be recognized that temperature fluctuations are frequently observed in these patients. 

The enteric nervous system is another division of the ANS. Disruption may result in clinically significant ileus and in severe cases, bowel perforation! In this setting, it may be helpful to consider either replacing opioids or stopping them altogether. Prokinetic agents like neostigmine may be considered dangerous in the setting of vagal hyperactivity due to an increased risk of bradyarrhythmia or asystole. Maximizing gastric motility with the use of enemas and stool softeners along with opioid-antagonists may be helpful. If all else fails and colonoscopy is unavailable, manual dis-impaction may be the only way to decompress. Get in there!

The Debrief

Dysautonomia is a complicated disorder that can have serious implications on inpatient mortality in the critical care setting. This disorder of the autonomic nervous system requires a careful, patient-centered, and multi-modal approach to effectively manage this condition and prevent further morbidity and mortality.

References

  1. Artal FJC (2017) Infectious diseases causing autonomic dysfunction. Clin Auton Res 28(1):67–81. PMID: 28730326.
  2. Meyfroidt G, Baguley IJ, Menon DK (2017) Paroxysmal sympathetic hyperactivity: the storm after acute brain injury. Lancet Neurol 16:721–729. PMID: 28816118.
  3. Rabinstein AA, Benarroch EE (2008) Treatment of paroxysmal sympathetic hyperactivity. Curr Treat Options Neurol 10:151–157. PMID: 18334137.
  4. Truax BT (1984) Autonomic disturbances in the Guillain–Barré syndromé. Semin Neurol 4:462–468. PMID
  5. Ropper AH (2003) Critical care of Guillain–Barré syndrome. In: Ropper AH (ed) Neurological and neurosurgical intensive care. Lippincott Williams & Wilkins, Philadelphia
  6. McLeod JG. Invited review: autonomic dysfunction in peripheral nerve disease. Muscle Nerve. 1992;15(1):3–13. PMID: 1310158.
  7. Cannon WB: Organization for physiological homeostasis. Physiol Rev 9:399, 1929.
  8. Elefteriou F: Impact of the autonomic nervous system on the skeleton. Physiol Rev 98:1083, 2018. PMID: 29717928.

Share:

More Posts

Related Posts

0
Would love your thoughts, please comment.x
()
x