The Abandoned Prisoner
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Cairns Base Hospital Cairns, Australia September, 2014 |
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The Tale
We begin our story with a quiet and rather introverted 39 year old prisoner who for the last several years had been residing in a high-security facility in northern Queensland; I know little of the reason for his incarceration and it is not relevant to the series of events described herein. The poor fellow had been found one morning drowsy, vomiting, and completely paralyzed on his left side, and was promptly sent in to our hospital.
My colleague was taking calls that day and he started the workup. Since the armed guard escorting our patient was unable to provide any history and there were no witnesses available, there was little to be gained through discussion. Examination revealed a young man of Indigenous Australian ancestry. His blood pressure was over 200 mmHg systolic - high. He was drowsy with a left homonymous hemianopia (a loss of the visual field on either side) as well as left hemispatial neglect (a deficit in attention to and awareness of one side of space that is not due to a lack of sensation). Moreover, complete weakness and sensory loss involving the left face, upper and lower limbs was noted. A computed tomography (CT) scan (a three dimensional x-ray) of the head promptly discovered the source of his ailment.
My colleague was taking calls that day and he started the workup. Since the armed guard escorting our patient was unable to provide any history and there were no witnesses available, there was little to be gained through discussion. Examination revealed a young man of Indigenous Australian ancestry. His blood pressure was over 200 mmHg systolic - high. He was drowsy with a left homonymous hemianopia (a loss of the visual field on either side) as well as left hemispatial neglect (a deficit in attention to and awareness of one side of space that is not due to a lack of sensation). Moreover, complete weakness and sensory loss involving the left face, upper and lower limbs was noted. A computed tomography (CT) scan (a three dimensional x-ray) of the head promptly discovered the source of his ailment.
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Here is part of the top of the brain (left on the scan equates to the right side of the brain and vice versa). You don't have to be an expert to see the area of hyperdensity (brighter compared to the rest of the brain tissue) on the right side of the brain. This is an intracerebral hemorrhage (bleeding within the brain tissue). Intracerebral hemorrhages usually result from uncontrolled hypertension (high blood pressure) and blood vessel rupture.
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Further down the brain, we can see that this hemorrhage is quite large. In fact, it is stretching the surrounding brain tissue and compressing the right lateral ventricle (a C-shaped structure that houses cerebrospinal fluid).
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As we look even further down, it is clear that the hemorrhage has leaked into the cerebrospinal fluid and there is blood in the fourth ventricle (the most inferior of the ventricles in the brain). This can be a foreboding sign.
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The CT scan was concerning, to say the least. Aside from the obviously large size of this bleed, there was evidence of mass effect (the effect of a growing mass that results in secondary pathological effects by pushing on or displacing surrounding tissue); mass effect may be lethal if the brainstem is compressed enough. The presence of blood in the fourth ventricle was especially concerning, for obstruction of that particular ventricle results in hydrocephalus (an abnormal accumulation of cerebrospinal fluid within the ventricles) which can crank up the intracranial pressure, also triggering brainstem compression.
My colleague showed me the CT scan and we both considered it. On the negative side, the bleed was big with evidence of mass effect. However on the positive side, the neocortex (the thin 2-3 mm strip of brain tissue enveloping the rest of the brain) was spared, meaning that if our prisoner survived this bleed, his 39-year old brain had a good chance of recovering some of the loss in vision and power. We both agreed that such a young man needed to be given every opportunity to recover and so my colleague called our Intensive Care Unit (ICU) and he was admitted there for blood pressure control and a mannitol infusion. My colleague then discussed the case with the nearest neurosurgery unit, located 350 kms away. It should have been a "no-brainer"; a young man with a survivable bleed should be transferred to a neurosurgery unit so that if hydrocephalus develops the pressure can be relieved to avoid brainstem compression, and a life saved.
Astonishingly, my colleague was rebuffed by both the neurosurgeons as well as the intensivists in their hospital. They looked at the CT scan and, based on their own reasoning, decided that our patient was not going to make it. There were a few lengthy discussions, but in the end no amount of convincing was going to make a difference here. Having done his best, my colleague left the patient with our own ICU and, as he had to fly interstate next morning, transferred the care of the afflicted patient to myself. Before leaving, he ordered a computed tomography angiography (CTA) scan (use of an injected contrast agent to outline the blood vessels) to make sure there were no obvious structural problems with the blood vessels; the CTA was normal.
Having been rebuffed by the neurosurgeons and their intensivists, things went from bad to worse for our poor prisoner. His Glasgow Coma Scale (GCS), which had been a steady 12, declined over the rest of the day to a 7. The GCS is a quantifiable scale used to measure the level of consciousness or awareness of an individual after a brain injury. The score is based on the addition of the scores from three separate tests - how well the patient's eyes open, how well they verbalize, and how well they move their limbs. The highest score is 15, which translates to a fully conscious or aware individual. The lowest score is a 3, which translates to a completely comatose individual. Thus, a 7 is not great. The intensivists in our own ICU repeated the CT scan early the next morning.
My colleague showed me the CT scan and we both considered it. On the negative side, the bleed was big with evidence of mass effect. However on the positive side, the neocortex (the thin 2-3 mm strip of brain tissue enveloping the rest of the brain) was spared, meaning that if our prisoner survived this bleed, his 39-year old brain had a good chance of recovering some of the loss in vision and power. We both agreed that such a young man needed to be given every opportunity to recover and so my colleague called our Intensive Care Unit (ICU) and he was admitted there for blood pressure control and a mannitol infusion. My colleague then discussed the case with the nearest neurosurgery unit, located 350 kms away. It should have been a "no-brainer"; a young man with a survivable bleed should be transferred to a neurosurgery unit so that if hydrocephalus develops the pressure can be relieved to avoid brainstem compression, and a life saved.
Astonishingly, my colleague was rebuffed by both the neurosurgeons as well as the intensivists in their hospital. They looked at the CT scan and, based on their own reasoning, decided that our patient was not going to make it. There were a few lengthy discussions, but in the end no amount of convincing was going to make a difference here. Having done his best, my colleague left the patient with our own ICU and, as he had to fly interstate next morning, transferred the care of the afflicted patient to myself. Before leaving, he ordered a computed tomography angiography (CTA) scan (use of an injected contrast agent to outline the blood vessels) to make sure there were no obvious structural problems with the blood vessels; the CTA was normal.
Having been rebuffed by the neurosurgeons and their intensivists, things went from bad to worse for our poor prisoner. His Glasgow Coma Scale (GCS), which had been a steady 12, declined over the rest of the day to a 7. The GCS is a quantifiable scale used to measure the level of consciousness or awareness of an individual after a brain injury. The score is based on the addition of the scores from three separate tests - how well the patient's eyes open, how well they verbalize, and how well they move their limbs. The highest score is 15, which translates to a fully conscious or aware individual. The lowest score is a 3, which translates to a completely comatose individual. Thus, a 7 is not great. The intensivists in our own ICU repeated the CT scan early the next morning.
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Not much change near the top of the brain; looks the same as the scan from the day before.
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Here is the problem. The intracerebral hemorrhage has clearly increased in size and there is even more mass effect than there was before. The right ventricle is now absent, and even the left ventricle is compressed. The increased pressure on the brainstem from above is affecting the structures responsible for generating arousal, resulting in the extreme drowsiness and GCS of 7.
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On a brighter note, the blood in the fourth ventricle has vanished; we can be a little less worried about hydrocephalus now.
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Based on their view that the outlook for our patient was poor now, with a good chance of dying, our ICU moved him back to the ward that morning. Our patient had had been abandoned yet again. I had a neurology clinic that morning but was notified of this decision by one of the intensivists.
I left clinic and went down to our stroke unit to see the man. His GCS was indeed 7; he did not open his eyes, nor did he speak at all, and he could only make faint localizing movements with his arms and legs. His breathing sounded bad, with "gurgling" noises occurring with every breath. While they may have sounded gruesome, such noises are usually a result of upper airway secretions and not a sign of real danger. They were probably contributed to in no small part by the highish rate of intravenous fluid replacement our fellow was receiving, as well as the fact that his nasogastric tube (a tube that goes through the nose into the stomach, used to protect the airway as well as for feeding) through which he was getting nasogastric feeds was out of position, possibly sending some of the feeds into his lungs. We turned the fluids down to a slow trickle, repositioned the nasogastric tube, and instituted regular and frequent suctioning of the upper airway to remove the secretions. I also stopped the feeds for a couple of days. He was already on antibiotics for an aspiration pneumonia (an acute inflammation of the lungs and bronchi resulting from foreign materials, such as food, entering the bronchi) that had presumably developed prior to or during his stay in ICU; I tinkered with these a little.
I was still optimistic for our prisoner, for a few reasons. First, although the bleed was big, but with his slow rate of decline in GCS it appeared to be approaching its maximum size. Second, despite being near that maximum size, the GCS was staying at a 7, not declining further to a 3. Third, he was young and the neocortex spared; young brains usually recover well, even with severe damage. Unfortunately, it was clear that we were on our own and would have to manage this fellow on our stroke unit.
Over the next few days, I visited our patient several times a day, mainly just trying to get on top of and optimize his blood pressure, fluid management, sodium levels, and aspiration pneumonia. The stroke nurses did most of the heavy lifting by setting up one-on-one nursing care and frequently suctioning his airway to remove debris. An armed guard was always present; it seemed kind of pointless, since our prisoner was not going anywhere in his state. After about two weeks of intensive management on the stroke unit he became mush less drowsy, and his GCS slowly picked up to an 11.
The most dangerous part of this ordeal was over - our prisoner, abandoned by many as a result of his large intracerebral hemorrhage secondary to uncontrolled hypertension, was going to survive.
I left clinic and went down to our stroke unit to see the man. His GCS was indeed 7; he did not open his eyes, nor did he speak at all, and he could only make faint localizing movements with his arms and legs. His breathing sounded bad, with "gurgling" noises occurring with every breath. While they may have sounded gruesome, such noises are usually a result of upper airway secretions and not a sign of real danger. They were probably contributed to in no small part by the highish rate of intravenous fluid replacement our fellow was receiving, as well as the fact that his nasogastric tube (a tube that goes through the nose into the stomach, used to protect the airway as well as for feeding) through which he was getting nasogastric feeds was out of position, possibly sending some of the feeds into his lungs. We turned the fluids down to a slow trickle, repositioned the nasogastric tube, and instituted regular and frequent suctioning of the upper airway to remove the secretions. I also stopped the feeds for a couple of days. He was already on antibiotics for an aspiration pneumonia (an acute inflammation of the lungs and bronchi resulting from foreign materials, such as food, entering the bronchi) that had presumably developed prior to or during his stay in ICU; I tinkered with these a little.
I was still optimistic for our prisoner, for a few reasons. First, although the bleed was big, but with his slow rate of decline in GCS it appeared to be approaching its maximum size. Second, despite being near that maximum size, the GCS was staying at a 7, not declining further to a 3. Third, he was young and the neocortex spared; young brains usually recover well, even with severe damage. Unfortunately, it was clear that we were on our own and would have to manage this fellow on our stroke unit.
Over the next few days, I visited our patient several times a day, mainly just trying to get on top of and optimize his blood pressure, fluid management, sodium levels, and aspiration pneumonia. The stroke nurses did most of the heavy lifting by setting up one-on-one nursing care and frequently suctioning his airway to remove debris. An armed guard was always present; it seemed kind of pointless, since our prisoner was not going anywhere in his state. After about two weeks of intensive management on the stroke unit he became mush less drowsy, and his GCS slowly picked up to an 11.
The most dangerous part of this ordeal was over - our prisoner, abandoned by many as a result of his large intracerebral hemorrhage secondary to uncontrolled hypertension, was going to survive.
The Condition
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An intracerebral hemorrhage involves bleeding within the brain tissue and commonly results from hypertensive damage to blood vessel walls (usually from primary hypertension or drugs), but bleeding can also occur from a vascular anomaly (aneurysm or arteriovenous malformation), arteriopathy (cerebral amyloid angiopathy or moyamoya), hemorrhagic necrosis (tumour, vasculitis, or infection), venous outflow obstruction (venous sinus thrombosis), or excessive cerebral blood flow (reperfusion injury or hemorrhagic transformation).
Clinically, focal neurological deficits are common. Around half of all patients display a reduced level of consciousness or awareness, nausea or vomiting, and headache. Rarely, in 6-7% of patients, acute seizures occur (Vespa et al, 2003). Treatments vary with the etiology, but blood pressure lowering with intravenous antihypertensives, mannitol infusions (a crystalline solid that osmotically reduces intracranial pressure), coagulopathy correction (with one or more of prothrombinex, fresh frozen plasma, vitamin K, or platelets), and seizure prophylaxis with intravenous anti-epileptics patients with lobar hemorrhages are nearly universal. The prognosis of intracerebral hemorrhage is not the best, with nearly half of all patients dying within the first month (Castellanos et al, 2005). A better outcome is seen with smaller, lobar bleeds with no intraventricular extension, as opposed to larger, deeper bleeds with intraventricular extension. |
Intracerebral hemorrhage may result when an aneurysm (a blood-filled bulge in the wall of a blood vessel) ruptures; aneurysm rupture is also commonly associated with subarachnoid hemorrhage.
Intracerebral hemorrhage may result from cerebral amyloid angiopathy (a disease where fibrous proteins are deposited into the walls the blood vessels, making them brittle and unable to contract properly). Cerebral amyloid angiopathy is extremely common in patients with dementia and one study diagnosed it at autopsy in 83% of 117 patients with confirmed Alzheimer's disease (Ellis et al, 1996)..
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Epilogue
Our prisoner slowly recovered over the next several months. As the bleed disappeared and the associated medical issues resolved, his GCS returned to 15. He was then subjected to intensive rehabilitation by a number of physiotherapists, occupational therapists, speech pathologists, and dieticians. While his visual loss and neglect partially recovered, at the time of writing this four months later, he had only recovered a bit of strength and still required a wheelchair to move around. I had hoped for more recovery. Still, he was able to communicate normally and move around using his wheelchair, which made all the difference to his family, especially his children.
During his rehabilitation, he applied for parole and is awaiting approval as I write this. The chances are good that he will get it.
Patients should not be abandoned by clinicians based largely on the appearance of a CT scan.
During his rehabilitation, he applied for parole and is awaiting approval as I write this. The chances are good that he will get it.
Patients should not be abandoned by clinicians based largely on the appearance of a CT scan.
References
Castellanos et al. 2005. Predictors of good outcome in medium to large spontaneous supratentorial intracerebral hemorrhages. Journal of Neurology, Neurosurgery, and Psychiatry 76, 691-695.
Ellis et al. 1996. Cerebral amyloid angiopathy in the brains of patients with Alzheimer's disease: the CERAD experience, part XV. Neurology 46(6), 1592-1596.
Vespa et al. 2003. Acute seizures after intracerebral hemorrhage: a factor in progressive midline shift and outcome. Neurology 60(9), 1441-1446.
Castellanos et al. 2005. Predictors of good outcome in medium to large spontaneous supratentorial intracerebral hemorrhages. Journal of Neurology, Neurosurgery, and Psychiatry 76, 691-695.
Ellis et al. 1996. Cerebral amyloid angiopathy in the brains of patients with Alzheimer's disease: the CERAD experience, part XV. Neurology 46(6), 1592-1596.
Vespa et al. 2003. Acute seizures after intracerebral hemorrhage: a factor in progressive midline shift and outcome. Neurology 60(9), 1441-1446.
