Clinical Signs and Prognosis

(1000 Patients evaluated within first 24 hours of coma)
*D/PVS *SD *MR/GR

Coma   sum      >11     12%     6%     82%
      3 or 4     87%     6%     7%

Pupils Nonreacting     39%     11%     50% 
       Reacting        91%     5%      4% 

Eye movements Latent     33%     11%     56% 
              Absent     90%     5%      5% 

c. Duration: Several studies have shown that the prognosis is reflected by the length of time the patient remains in a coma.

(ii) Criteria - Criteria have been developed which diagnose with certainty that brain death has occurred. These are:

a. unreceptivity and unresponsivity - total unawareness of external and internal stimuli; no response to pain.

b. no movement or breathing - observation at least one hour with no spontaneous movement; apnea for three minutes.

c. absence of cephalic reflexes. Cephalic responses are defined as:

pupillary - any direct or consensual response of the pupil to bright light;

corneal - unilateral or bilateral blink by touching each cornea with a wisp of cotton;

oculocephalic (doll's eyes) - contraversive conjugate eye deviation produced by brisk passive movement of the head from side to side (if absent, eyes remain centered in primary position);

caloric response (vestibular) - nystagmus or ocular deviation induced by ice water gently syringed into external auditory canal;

pharyngeal (gag reflex) - contraction of constrictors of pharynx or elevation of palate in response to touching posterior pharynx;

postural activity - decerebrate or decorticate posturing;

stretch (tendon reflex) - elicited on each side, biceps, triceps, radial, knee and ankle.

For brain death to be diagnosed all of the above criteria must be met. Also note that a flat EEG does not preclude recovery.

Even with the best attention and medical facilities 60-80 per cent of patients in coma for more than six hours do not make a recovery to an independent existence. The comatose patient suffers considerably while comatose. Those patients that emerge from coma continue to suffer from a myriad of neuropsychological abnormalities.

A score of 12 to 13 is mild, 9 to 11 is moderate, and 8 or less indicates severe brain damage. The severity of coma correlates with the severity of diffuse axonal injury. Brian exhibited a GCS score at the scene of the accident of 9. Upon admission to Memorial, that scale score was a 6. At approximately 10:30 p.m. on the night of the incident his GCS score was down to 3, which is indicative of near brain-death.

c) Subarachnoid Hemorrhage in Interpeduncular Fossa

A CT scan ordered by Dr. Benjamin Trujillo upon admission to Memorial on August 25, 1997, revealed a post-traumatic subarachnoid hemorrhage in the interpeduncular fossa and multi-focal contusions including a possible brain-stem contusion. The CT scan revealed that intracranially there were areas of hemorrhagic contusion at the right frontoparietal vertex in the left lobe frontal area. Additionally, there were amounts of post-traumatic subarachnoid hemorrhage seen in the interpeduncular fossa.

d) Intracranial Pressure

Hypertension is an indication of advancing increased intracranial pressure. An elevated blood level of carbon dioxide results in sympathetic stimulation, which produces vasoconstriction and thereby an increase in arterial blood pressure. In response to cerebral ischemia, blood pressure may rise to 270mm Hg and produce extensive peripheral vasoconstriction so intense that blood vessels become obliterated. Brian experienced such intracranial pressure immediately after the accident, which, in the absence of the Camino Bolt, could have caused tragic results including total blindness and possibly death.

Neurosurgeon, Dr. Frank Waterhouse, was brought in for consultation and evaluation of the CT scan. After reviewing the CT scan, Dr. Waterhouse noted elevated intracranial pressure and closed head injuries. Dr. Waterhouse then ordered emergency surgery for placement of a right frontal Camino Bolt to monitor Brian's intracranial pressure because of his closed head injuries. The intracranial pressure monitor was successfully placed in Brian's right frontal region.

e) Subdural Hematoma

Dr. Trujillo noted an interhemispheric subdural hematoma present on the right side of the falx at the vertex in Brian's radiology charts. Subdural Hematoma consists of a collection of liquid which in turn is composed of a variable composite of blood and/or cerebrospinal fluid, situated between the dura and the outer surface of the leptomeninges. This site between the dural membrane and the arachnoid membrane covering the brain and spinal cord is the subdural space. Since no communication exists between the subdural space and the subarachnoid space in which the cerebrospinal fluid circulates, hemorrhage occurring into the subdural space produces trapping of the blood with subsequent formation of a blood clot (hematoma). This hematoma has the capacity for behaving like a mass space-occupying lesion, causing compression of the underlying brain, and necessitating surgical intervention in order to remove the hematoma.

The collection of fluid beneath the dura in a subdural hemorrhage may vary considerably as to size, extent, and rapidity of development, and therefore there are three admittedly arbitrary groupings: 1) acute; 2) subacute; and 3) chronic. A subdural hematoma is acute when symptoms occur within three days following injury, subacute when symptoms present within four to twenty days, and chronic when there have been no symptoms until more than twenty days have elapsed since the injury. Brian presented with an acute subdural hematoma as his hematoma was diagnosed initially upon admission to Memorial.

The mortality rate reported with acute subdural hematomas is high: fifty to seventy percent, One again indicating the life- threatening nature of the injuries visited upon Brian by the negligence of James Anderson.

f) Right Frontal Brain Lobe Subcortical Shear

On November 12, 1997, Dr. Gerard Quiznos, Brian's primary care physician at B.R.R.I., ordered an MRI of the brain due to Brian's slow recovery of his cognition. The MRI examination revealed evidence of a shear injury from the head trauma involving the right frontal lobe. There was moderate to severe ventriculomegaly involving the lateral and third ventricles. Downward compression of the optic chiasm was noted related to the enlarged third ventricle. The ventricles demonstrated a periventricular halo, especially at the frontal and occipital margins. A flow void was demonstrated through the cerebral aqueducts which was evidence of T2 hypointensity involving the right frontal lobe compatible with Brian's prior history of right frontal shear injury arising out of the collision.

g) Hydrocephalus

Findings from the MRI performed on November 12, 1997, were suggestive of communicating uncompensated hydrocephalus secondary to the subarachnoid hemorrhage and evidence of a shear injury involving the right frontal lobe. Hydrocephalus is characterized by an increase in the quantity of cerebrospinal fluid in the brain and the dilation of the cerebral ventricles under pressure. The etiology includes the following:

(i) Failure in the absorption system;
(ii) Excessive production of cerebrospinal fluid; and
(iii) Obstruction of the system between the source of cerebrospinal fluid production and the area of its reabsorption (the obstruction may be partial, intermittent or complete).

The types of hydrocephalus include internal and external, the latter of which is rare. Internal hydrocephalus includes:

(i) Non-communicating hydrocephalus, which is an obstruction located within or at the outlets of the ventricular system, preventing any or all of the cerebrospinal fluid from leaving the ventricles and entering the subarachnoid space; and
(ii) Communicating hydrocephalus, in which there is free communication between the ventricles and the subarachnoid space, and abnormal reabsorption of the cerebrospinal fluid in the subarachnoid space occurs.

Clinically, patients with hydrocephalus develop headaches, vomiting, and confusion, which gradually progresses, unless treated, to frank mental retardation.

Dr. Anthony Curtis of St. Elmo's Episcopal Hospital was consulted for treatment of Brian's hydrocephalus. In an operation performed on November 18, 1997, Dr. Curtis placed a right parietotemporal ventriculoperitoneal shunt to alleviate the pressure on the brain.

The shunt consists of a tube with a one-way valve which is inserted surgically to lead cerebrospinal fluid from the brain directly into some other body cavity. The procedure reduces the volume and thus the pressure of the cerebrospinal fluid within the ventricles. The ventriculoperitoneal shunt in Brian's brain diverts cerebrospinal fluid from a lateral ventricle or the spinal subarachnoid space to the peritoneal cavity. A tube is passed from the lateral ventricle through an occipital burr hole subcutaneously through the posterior aspect of Brian's neck and perospinal region to the peritoneal cavity through a small incision in the right lower quadrant of the abdomen. The reservoir is placed under Brian's scalp just behind the ear, or through a burr hole, in order to tap the lateral ventricle. The reservoir can be punctured through the scalp with a large Huber needle to irrigate and clear an obstruction in the ventricular catheter, to introduce a contrast medium for an x-ray check of the patency, to inject medication into the ventricle, or to serve as a flushing device when digital compression is applied.

In Brian's case, a small curvilinear incision was mapped out on the right parietotemporal area of the head just above and behind the right ear. Initially, a transverse, right upper quadrant abdominal incision was made and then the peritoneum was exposed via muscle and fascia splitting incision, and the peritoneum was opened and a small pursestring stitch was placed in the peritoneal opening. Next, the curvilinear incision of the cranium was opened sharply. After cauterizing and opening the dura, Dr. Curtis noted that the exposed cortical brain area was bulging slightly from a small dural opening, indicating at least somewhat increased intracranial pressure from the hydrocephalus. After placing a distal abdominal shunt catheter tubing between the two incisions, the entire system was filled with normal saline irrigation and the ventricular catheter tubing was inserted into the right lateral ventricle through the same needle tract and the shunt bubble pumped and refilled normally.

After the successful surgery, Brian was transferred back to B.R.R.I. on November 20, 1997.

h) Partial Blindness - Right and Left Eyes

Brian repeatedly complained of partial blindness during his hospitalization at both St. John and B.R.R.I. On December 17, 1997, while at TLC, Brian was examined by Dr. Arthur G. Horowitz, a neuroophthalmologist at Seeview Eye Consultants. Among other injuries, Brian was noted to have a right visual field cut which is partial blindness in both eyes. Particularly, Dr. Horowitz stated:

[Brian] suffered a traumatic brain injury and has a right incongruous denser superiorly homonymous hemianopsia associated with a right afferent pupillary defect and right sided band atrophy, consistent with damage to the left optic tract. He had hydrocephalus and may have suffered post-papilledema or post-hydrocephalus optic atrophy.

Dr. Roscoe N. Gray, the former surgical director emeritus of Aetna Casualty and Surety Company explained homonymous hemianopsia as causing blindness in the temporal field of the right eye and the nasal field of the left eye. He explained that homonymous hemianopsia is caused by a lesion to the optic tract behind the optic chiasm. In Brian's case, Dr. Horowitz explain that he had damage to the left optic tract, which would explain the right-sided homonymous hemianopsia, i.e., blindness in the right field of vision of each eye.

It is apparent after Brian's visit with Dr. Horowitz that he is fortunate to have any of his eyesight. If Dr. Waterhouse had not timely inserted the Camino Bolt to relieve the intracranial pressure in Brian's cranium, complete blindness would have been the natural consequence of his subarachnoid hemorrhage and resulting hematomas.

Dr. Horowitz ordered a follow-up neuroimaging study in addition to fitting Brian with hemianoptic prism spectacles. Brian's partial blindness interferes with his concentration and ability to interact on an everyday basis. This injury alone is sufficient to keep Brian from ever being a safe driver because of his lack of peripheral vision on the right side.

i) Papilledema

Dr. Horowitz indicates that Brian suffered post-papilledema optic atrophy. Dr. Gray explains the consequences of papilledema with the following description:

The optic nerve may be compressed as a result of increased intracranial pressure, causing a condition known as papilledema or choked disc. The anatomic arrangement of the three meningeal coverings of the brain which also invest the optic nerve permits increases in intracranial pressure to be transferred through the cerebrospinal fluid to the subarachnoid space around the optic nerve. In this arrangement, the outer layer, or dura, of the brain merges with the outer coat of the eyeball while the subarachnoid space of the intracranial cavity is continuous with the subarachnoid space around the optic nerve. Increased intracranial pressure causes the central retinal vein to be compressed and engorges the intraocular veins causing swelling of the papilla, or optic disc. The signs of this occurrence are diminished visual acuity, a disc pinker than normal, a less sharply defined disc, whitish patches of exudate, and flame-shaped hemorrhages. As the swelling progresses, the surface of the disc becomes elevated above the level of the surrounding retina and the visual fields begin to constrict concentrically with diminishing acuity. If pressure is not relieved, blindness will be the ultimate result, if the increased intracranial pressure or its proximate impelling condition does not prove fatal first. (emphasis added)

j) Optic Atrophy

Atrophy is a decrease in size of an organ or part due to shrinkage of its constituent cells. Dr. Horowitz also noted that Brian suffered from right-sided band atrophy, indicative of partial or complete death of the optic nerve, which will destroy sight. The optic nerve does not regenerate after injury to its fibers and optic atrophy results.

Dr. Horowitz also noted post-papilledema which is a sign of increased intracranial pressure often indicating an intracranial hematoma. This is consistent with Brian's initial diagnosis upon admission to Memorial.

k) Hearing Impairment - Right and Left Ears

On March 3, 1998, Brian went to an otolaryngologist for hearing loss. Dr. Chang performed an audiogram on Brian which revealed sensorineural hearing loss at 4 kHz. He indicated that the hearing loss was likely due to the trauma resulting from Brian's tragic incident. At this time, there is nothing further that Dr. Chang can do for Brian.

l) Multiple Ruptured Cervical Discs

Dr. Galloway ordered an MRI of Brian's cervical spine on February 16, 1998, due to his continuing complaints regarding neck pain. The MRI revealed ventral spondylosis at C2-3 with mild ventral spondylosis at C4-5; a broad-based posterocentral protrusion measuring approximately 2-3 mm at C3-4; a broad-based posterocentral protrusion measuring 2-3 mm at C4-5 which abuts but does not cause focal indentation upon the cervical cord; and a broad-based posterocentral protrusion measuring approximately 2-3 mm at C5-6 which abuts and may cause minimal indentation on the ventral margin of the cervical cord.

At this point in time, Brian will continue to see Dr. Anthony Curtis, his treating neurosurgeon, for further treatment including a potential CT myelogram or possibly surgical intervention.

m) Right Colonic Mesentery Tear

Upon arrival at Memorial, Brian's initial evaluation by Dr. Benjamin Trujillo revealed evidence suggestive of intra-abdominal injury. Dr. Trujillo performed a diagnostic peritoneal lavage which returned a bloody effluent containing 250,000 red blood cells per cc of fluid. He was emergently taken to the operating room for an exploratory laparotomy. After the orthopedic service completed placement of the femoral pin in his right hip, Dr. Benjamin Trujillo and Dr. Todd Rogers performed the exploratory laparotomy which revealed blunt injury to the right colon including tears of the right colon mesentery.

Two areas of the right colon revealed focal necrosis, along with a small area of serosal tear along the hepatic flecture of the colon. Dr. Trujillo then performed the colon resection of approximately two centimeters of the terminal ilium with resection of the cecum, right colon to an area just proximal to the middle colic vasculature. Once the hemicolectomy was complete, the remainder of the abdominal exploration revealed no evidence of hepatic injury. Dr. Trujillo then placed a feeding jejunostomy tube into Brian because of the suspected need for long-term feeding. Brian was taken to the intensive care unit after tolerating the surgery well.

n) Herniated Nucleus Pulposi - Lumbar

Brian has been experiencing numbness radiating down his right leg which indicates damage to a disc at the L4-5/L5-6 level. Although he has not had an MRI of his lumbar region performed, his symptoms indicate herniated nucleus pulposi. As soon as is practical, an MRI will be performed on Brian's lumbar region and we will report the results.

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