Dear Bloggers
I wanted to impart to you a rather rare case of a patient who had a history of spinal cord injury and who developed accelerated hypertension and cold upper extremities.
This male patient had a C-spine fracture and transection of the spinal cord 5 yrs before following a fall and he was left with quadriplegia and reliant on mechanical ventilation to breath.
He was normally otherwise well albeit fully dependent.
On the evening of admission, the patient developed a low grade fever but otherwise had no new symptoms.
The blood pressure was noted to be 220/110 mmHg and his carer noticed that his hands and arms were very cold to the touch.
He was admitted to the hospital via the emergency medical services.
There was no other other relevant medical history and the patient was taking no regular medications.
There was no relevant family history.
The patient was cared for at home and was nursed 24 hours a day on a pressure bed and had home mechanical ventilation. The patient was fed via PEG tube and required full help with toileting.
On examination
The patient was fully alert and was able to speak albeit softly. Temp 37.5 degrees C.
HEENT examination was grossly intact.
Cardiac: pulse 74/min, BP 220/110 mmHg, JVP not elevated, Heart Sounds 1 + 2. No added sounds and no murmurs.
Resp: RR= 14/min (ventilator setting), tracheostomy in vivo, spO2 98%, expansion equal, percussion resonant, chest sounds clear.
Abdomen: Soft, flat, non-tender (remember patient has spinal cord transection), no obvious masses, normal bowel sounds. Rectal examination not performed.
Extremties - DVT prevention stockings on both legs. No oedema, redness or pain.
Cranial Nerves: II - normal, pupils equal and reactive to light and accommodation. III, IV, VI - normal extra-ocular movements, V- normal motor and sensory modalities. VII - normal. VIII- normal, IX, X, XI - no gross abnormalities, XII - normal tongue movement.
PNS - Power 0/5 throughout all limbs, absent sensation up to C3 level, Babinski bilaterally extensor.
Laboratory
Lab studies were generally normal except for a slight rise in the WBC count of 12 x 10-9/L Urine analysis revealed turbid urine. WBC >100 / hpf, RBC 5-10 / hpf, nitrites +, protein 2+, bacteria 4+ (gram stain: Gram Negative Bacilli).
Urinary catheterisation revealed 1 L of urine in the bladder.
CXR - NAD
ECG - 74/min, no focal abnormality.
Diagnosis
The diagnosis here is obviously a urinary tract infection with urinary retention.
However, why did the patient develop hypertension and peripheral vasoconstriction?
The answer is unique to spinal cord injury patients and it is termed Autonomic Dysreflexia.
Certain noxious stimuli such as Urinary Retention (associated with UTI), impaction of stool within the bowel, pressure sores, fractures or intra-abdominal disease lead to a dysfunction of the autonomic responses of the heart and vascular contractility. This lack of control of the sympathetic nervous system leads to vasoconstriction and hypertension. Interestingly, a parasympathetic response occurs above the level of the lesion albeit that it is not sufficient to offset the adverse actions of the sympathetic response.
This can occur in patients with spinal cord lesions above the T6 cord level and the frequency of those affected is variable. It is unusual in the immediate aftermath of injury but usually occurs within the first year.
Patients can present with various symptoms and signs and include:
I wanted to impart to you a rather rare case of a patient who had a history of spinal cord injury and who developed accelerated hypertension and cold upper extremities.
This male patient had a C-spine fracture and transection of the spinal cord 5 yrs before following a fall and he was left with quadriplegia and reliant on mechanical ventilation to breath.
He was normally otherwise well albeit fully dependent.
On the evening of admission, the patient developed a low grade fever but otherwise had no new symptoms.
The blood pressure was noted to be 220/110 mmHg and his carer noticed that his hands and arms were very cold to the touch.
He was admitted to the hospital via the emergency medical services.
There was no other other relevant medical history and the patient was taking no regular medications.
There was no relevant family history.
The patient was cared for at home and was nursed 24 hours a day on a pressure bed and had home mechanical ventilation. The patient was fed via PEG tube and required full help with toileting.
On examination
The patient was fully alert and was able to speak albeit softly. Temp 37.5 degrees C.
HEENT examination was grossly intact.
Cardiac: pulse 74/min, BP 220/110 mmHg, JVP not elevated, Heart Sounds 1 + 2. No added sounds and no murmurs.
Resp: RR= 14/min (ventilator setting), tracheostomy in vivo, spO2 98%, expansion equal, percussion resonant, chest sounds clear.
Abdomen: Soft, flat, non-tender (remember patient has spinal cord transection), no obvious masses, normal bowel sounds. Rectal examination not performed.
Extremties - DVT prevention stockings on both legs. No oedema, redness or pain.
Cranial Nerves: II - normal, pupils equal and reactive to light and accommodation. III, IV, VI - normal extra-ocular movements, V- normal motor and sensory modalities. VII - normal. VIII- normal, IX, X, XI - no gross abnormalities, XII - normal tongue movement.
PNS - Power 0/5 throughout all limbs, absent sensation up to C3 level, Babinski bilaterally extensor.
Laboratory
Lab studies were generally normal except for a slight rise in the WBC count of 12 x 10-9/L Urine analysis revealed turbid urine. WBC >100 / hpf, RBC 5-10 / hpf, nitrites +, protein 2+, bacteria 4+ (gram stain: Gram Negative Bacilli).
Urinary catheterisation revealed 1 L of urine in the bladder.
CXR - NAD
ECG - 74/min, no focal abnormality.
Diagnosis
The diagnosis here is obviously a urinary tract infection with urinary retention.
However, why did the patient develop hypertension and peripheral vasoconstriction?
The answer is unique to spinal cord injury patients and it is termed Autonomic Dysreflexia.
Certain noxious stimuli such as Urinary Retention (associated with UTI), impaction of stool within the bowel, pressure sores, fractures or intra-abdominal disease lead to a dysfunction of the autonomic responses of the heart and vascular contractility. This lack of control of the sympathetic nervous system leads to vasoconstriction and hypertension. Interestingly, a parasympathetic response occurs above the level of the lesion albeit that it is not sufficient to offset the adverse actions of the sympathetic response.
This can occur in patients with spinal cord lesions above the T6 cord level and the frequency of those affected is variable. It is unusual in the immediate aftermath of injury but usually occurs within the first year.
Patients can present with various symptoms and signs and include:
- headache
- nausea
- bradycardia or tachycardia
- sweating
- hypertension
- nasal congestion
- altered mental state e.g. anxious
Patients may exhibit no symptoms at all whereas others may develop profound bradycardia leading to cardiac arrest or hypertensive crisis causing intracerebral bleeding and convulsions.
Patients can be managed in several ways and include sitting them up to cause the BP to drop, searching for inciting stimuli (e.g. urinary outflow obstruction / UTI), acute reduction of BP (nitrates, peripheral calcium channel blocker, ACE-I, hydralazine, IV labetolol).
In this case, the history of spinal cord injury and the symptoms of peripheral vasoconstriction plus profound hypertension made the diagnosis of autonomic dysreflexia a certain diagnosis at the bedside and after the hunt for the inciting cause, a UTI and urinary outflow obstruction were found.
Treatment with urinary catheter insertion to relieve the obstruction and antibiotics caused the BP to drop within several hours, with a resting BP of 100/60 mmHg without the need for acute anti-hypertensive therapy. The perfusion to the upper limbs normalised spontaneously.
For more in-depth reading concerning patients with spinal cord injuries, please read UpToDate 16.2
Have a great day.... :-)
Patients can be managed in several ways and include sitting them up to cause the BP to drop, searching for inciting stimuli (e.g. urinary outflow obstruction / UTI), acute reduction of BP (nitrates, peripheral calcium channel blocker, ACE-I, hydralazine, IV labetolol).
In this case, the history of spinal cord injury and the symptoms of peripheral vasoconstriction plus profound hypertension made the diagnosis of autonomic dysreflexia a certain diagnosis at the bedside and after the hunt for the inciting cause, a UTI and urinary outflow obstruction were found.
Treatment with urinary catheter insertion to relieve the obstruction and antibiotics caused the BP to drop within several hours, with a resting BP of 100/60 mmHg without the need for acute anti-hypertensive therapy. The perfusion to the upper limbs normalised spontaneously.
For more in-depth reading concerning patients with spinal cord injuries, please read UpToDate 16.2
Have a great day.... :-)
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