SBS: SUBDURAL HEMATOMA (OTHER CAUSES)

SUBDURAL HEMATOMA

Subdural Hematoma is one of the three symptoms of the triad used to diagnose Shaken Baby Syndrome. According to the unproven SBS hypothesis, shaking causes the brain to impact against the inside of the skull, causing widespread brain damage (Diffuse Axonal Injury) and ripping (shearing) the veins between the brain and skull (bridging veins) resulting in bleeding (Subdural Hematoma) in the "subdural spaces" in between and behind the eyes (Retinal Hemorrhages).

However, this remains a concept without scientific support. In fact, the exact cause--mechanism of action--of retinal hemorrhages remains unknown. Subdural hematomas and retinal hemorrhages often occur together but there are times when subdural hemorrhages are found by themselves, and retinal hemorrhages occur alone also in accidental injuries and medical conditions unrelated to abuse or even traumatic forces,

The idea that the triad of symptoms is caused by shaking alone is nothing short of irresponsible misinformation and possibly medical malpractice leading to the tragedy of misdiagnosis with catastrophic legal consequences to caretakers and their families.

The shaking hypothesis evolved in the worst possible way, scientifically speaking. Decades ago Dr. Caffey read about an incident where an enormous, muscle-bound nurse admitted to shaking numerous infants and babies in her care, three of whom later died, although it wasn't proven that shaking was the cause of death.

Normally, to prove a hypothesis, other causes of the same symptoms must be identified (Differential Diagnosis) and eliminated. This never happened, which means the hypothesis was never proven. Even worse, a diagnosis is also made without eliminating other causes. In short, "shaking" was an assumption, not a fact.

Even before the idea of SBS was presented to the public in 1972, mechanical shaking experiments involving primates demonstrated that it would take around 155 g's of force to cause bleeding in the brain, and shortly after that it was proven that the normal person can only generate around 9 g's of force. Also, that violent shaking would cause neck injuries not seen in these cases. Now, injury biomechanical engineers have come right out and said SBS was was not possible as described because humans can't generate that kind of force. Even if they did violently shake an infant, neck injuries would be seen, and those could cause the symptoms, but only by damaging the brain stem and shutting off respiration and causing braining swelling, which in turn caused hemorrhaging, which is not the mechanism of action claimed by SBS "experts". Still, there would be neck injuries. No neck injuries, no assault by shaking.

"During one trial, the prosecution stated that infantile scurvy was no longer seen. I replied with ‘Yes it is. But it is not called ‘scurvy’, it is called the ‘shaken baby syndrome’." --Dr. Archie Kalokerinos, MD

Subdural Hematoma cause by Barlow's disease (Infantile scurvy) The relationship between vaccine-caused vitamin C deficiency, which is a hemorrhagic condition resulting from "capillary fragility" and subdural bleeding.

http://www.2ndchairservices.com/sbsdefense/?page_id=62
Alternate Explanations

The myth that children do not die from short falls is incorrect on its face. We know from published medical data, that perfectly healthy children die of short falls (1-4ft.). Furthermore, the myth that children don’t die of short falls, assumes that those children do not possess any intervening factors that would make them more fragile to a head injury. As a metaphor, it would generally be assumed, and supported by medical literature, that children do not die of paper cuts or minor external head wounds. This would, however, be defied by cases involving hemophiliacs. One would be in great error to assume that a child was abused simply because it was disparate from the norm, without paying careful attention to intervening factors. In SBS cases, doctors are generally unable, (because the baby is deceased) or uninterested, in pursuing other explanations for the injuries, once a diagnosis of SBS has been reached.

It needs to be made clear from the outset that we believe that short falls can and do kill healthy children. However, there are also several underlying medical conditions that can lessen the degree of force necessary to cause the injuries found in “SBS” cases:

“Chronic” or “old” subdural hematomas: An infant with an old or chronic subdural hematoma may suffer “rebleeds” with little or no impact at all. Witnesses for the State will generally argue that chronic subdural hematomas do not bleed or rebleed without force equal to or greater than that incurred in a 2-3 story fall. This testimony, however, is not supported by the literature on rebleeds.

Most of the literature available on chronic subdural hematomas is on hematomas in adults. However, for adults, it is generally assumed that chronic subdural hematomas, by their very nature, evolve and can rebleed over time. Though little has been published specifically about re-bleeding subdurals in infants, there there is extensive literature on chronic subdural hematomas in infancy. Further, it is assumed by most experts in the treatment field that the processes involved in production of a chronic subdural hematoma is the same, regardless of age. Studies have showed that the disruption in the organization of membranes created by the (resolving) subdural hematoma can often cause new hematomas to form. Most experts will agree, if pressed, that chronic subdural hematomas are likely to rebleed with little to no impact at all.

Case Note
BB was an 8-week-old infant that arrested 11 days after his second well-baby checkup. The child had been lethargic and refusing food for several days. The parents reported that he cried more when he was laid flat and that his cry was more nasal and whinier than normal. He had what could be interpreted as seizures and had been brought to the doctor with “raccoon eyes” the week before. The raccoon eyes (periorbital echymosis) were diagnosed as a vitamin K deficiency and treated with a shot of vitamin K. On the day the baby arrested, he had been taken to the emergency in the morning for projectile vomiting in the church daycare. Later that day, the baby arrested while in the care of the father (the mother was taking a bath). The paramedics arrived and took the child to the local hospital. They diagnosed him with reflux and told the parents he would have to stay overnight. Later that night when the baby started having seizures, he was taken to a trauma hospital in a nearby town. The CAT scans performed at this hospital revealed an acute subdural hematoma, evidence of an old subdural hematoma dating several weeks old and a unilateral retinal hemorrhage. The infant was sedated for several weeks and had regular CAT scans performed until his release. The CAT scans and MRIs showed the subdural hematoma spontaneously rebleed at periodic intervals throughout the six weeks the infant stayed in the hospital, and his intracranial pressure fluctuated over time as well. The case was tried by Michael Moore in Warner Robbin’s, Georgia. The jury acquitted in less than a half an hour.

Birth Trauma

Recent studies have show between 26-46% of all babies born have some form of intracranial hemorrhages on their brain (Rooks; Looney). Most go un-noticed and heal without ever becoming symptomatic, but some rebleed with a short fall, a bad vaccine, an infection, etc.

Hydrocephalus

Hydrocephalus, also called benign Cerebral Fluid of Infancy, literally water on the brain, is a generic term that covers several conditions:

External hydrocephalus: This is excessive cerebrospinal fluid-CSF over the brain with normal or relatively normal ventricle size.
Internal hydrocephalus: This is excessive CSF inside the ventricles of the brain. Clinical symptoms are similar to other closed head trauma; unsteady broad-based gait, history of falling, apathy, lethargy, inattentiveness, etc.

Hydrocephalus can be caused by several phenomena, as embodied in their names.

Obstructive or non-communicating hydrocephalus involves impedance to flow of CSF from or between the ventricular chambers in the brain and the brain’s surface. This can be due to prior viral or other infection with scarring of the exiting foramina at the base of the cerebellum, obliteration by scar, tumor, or some other process of the narrow connecting passages (foramina of Munro, aqueduct of Sylvius) between the ventricles within the brain.
Communicating hydrocephalus assumes that CSF can exit the brain, but there may be impedance due to scarring of the subarachnoid space, or scarring or other dysfunction of the arachnoid granulations where CSF is absorbed (possibly due to recent or remote subarachnoid hemorrhage). Combinations of all of the above may result in impaired transport or absorption of CSF relative to the amount produced by the brain. This may lead to increased intracranial pressure and complications from this.

Coagulopathies

The blood constantly exists in an equilibrium of clotting on the one hand, and anti-coagulation on the other. Disruption of this equilibrium leads to the condition of coagulopathy. Coagulopathy can have two faces: clotting in various locations or everywhere within the vessels, leading to deposition in a worst case of intravascular clots in the brain, lungs, kidneys and other organs (disseminated intravascular coagulation-DIC). Once clotting factors have been consumed or otherwise inactivated, spontaneous bleeding may occur anywhere in the body, but is most likely where some form of injury exists. There are many conditions, circumstantial, acquired and inherited, that can cause a dysfunction in clotting manifested in many ways. These conditions may not be all or none in their expressions.

An apparently uncommon, but probably under appreciated complication of coagulopathy, is thrombosis of the superior sagittal sinus (and/or other intradural venous sinuses) as well as cortical veins. In its most virulent form, affected individuals may suddenly decompensate with a rapid rise in intracranial pressure, subarachnoid and subdural hemorrhage, venous infarction and bleeding within the brain. Such individuals usually die. There may be lesser, more subtle forms of this process that may not be immediately or ever recognized. This may include intermittent or partial thrombosis of a major cortical draining vein with or without venous sinus thrombosis. The consequences of this can be headache, lethargy, seizures, irritability or prostration. There may be cerebral edema, subarachnoid hemorrhage, subdural hemorrhage, and sometimes, bleeding in the brain as well. Such individuals may also show retinal hemorrhages. These conditions may be caused, especially in young infants by dehydration (secondary to persistent vomiting, diarrhea, insufficient fluid intake), fever, infections and sepsis, brain trauma and a host of other conditions. Sagittal sinus and venous thrombosis may occur in conjunction with the “respirator” brain phenomenon and have nothing to do with any prior condition. A careful post-mortem examination can often differentiate whether the process is pre-mortem or intra-mortem.

Disseminated Intravascular Coagulopathies are a group of disorders that affect clotting or thrombosis. These disorders come in both genetic and acquired forms and are not easily diagnosed. Coagulation disorders produce increased vascular permeability and a decreased ability to clot after suffering a subdural hematoma. Unfortunately, because most of the clotting and complement disorders can only be tested on circulating blood, it is nearly impossible to determine retrospectively, during autopsy, whether a child had a clotting disorder that either exacerbated or caused a subdural hematoma.

Thrombocytopenia (TCP) is a coagulopathy defined by platelet counts of less than 100,000/mm of blood. Platelet counts of less than 50,000 have been associated with bleeds from minor trauma whereas platelet counts between 10,000-15,000 result in spontaneous hemorrhages. TCP can travel with other congenital conditions, such as TCP with Absent Radii (TAR) Syndrome, May Hegglin Syndrome, Wiskott-Aldrich Syndrome and Autosomal Recessive TCP. TCP can also be idiopathic. Ideopathic or immune TCP is caused by an autoimmune process which destroys platelets. It is found in 1 in 10,000 people. Ideopathic TCP is generally diagnosed from bruises or petichae on the body or mucosa sinuses, bleeding gums, epistaxis hematuria, menorrhagia, weight loss, fever and headache. Treatment includes prednisone or splenectomy. TCP has three major causes:

Decreased bone marrow production: This can be tested by bone marrow biopsy. It generally affects hemopoiesis, so it may be accompanied by varying degrees of anemia or leukopenia.
Splenic Sequestration Abnormalities: Check for an enlarged spleen. The most common cause is portal hypertension secondary to liver disease.
Accelerated Distraction: Abnormal vessels, fibrin thrombi or intravascular prostheses can all shorten the life span of a platelet and cause non-immunologic TCP.

Drug Induced TCP: Most patients recover within 7-10 days. Some more severely affected patients require platelet transfusions or temporary support with glucocorticoids or plasmapheresis. Patients are warned to avoid the offending drug in the future, because only “minute” amounts of the drug are needed to set up subsequent immune reactions. Heparin is highly suspect to cause TCP and TCP has been found to be more common in Heparin derived from beef lung. Vaccines have been shown to produce such results.

Idiopathic TCP: 90% of the pediatric cases of immunologic TCP are seen following a recovery from upper respiratory illness or from a “viral exanthem.” Acute idiopathic TCP generally recovers in 4-6 weeks though some cases take 3-6 months.

Thrombocythemia (i.e. Thrombocytosis) is a coagulopathy characterized by platelet counts greater than 400,000. Both forms of TCC can cause hemorrhages in the veins of the skin, stomach, eyes, brain and vital organs

Primary Thrombocythemia(TCC) is a condition where platelets are produced in greater number than usual.
Secondary Thrombocytopenia is more rare and more difficult to diagnose. It follows splenic atrophy, malignancy of the lungs, etc., or chronic blood loss.

Von Willebrands Disease (VWD) is the most common inherited bleeding disorder. This disorder, characterized by a decreased production of Von Willebrand factor, (VWF) does two things:

It facilitates platelet adhesion under conditions of high shear stress by linking platelet membrane receptors to vascular subendothelium. Normal VWF levels are 10mg/L. “A modest reduction in VWF concentration, or selective loss of high-molecule weight multimeters, decreases platelet adhesion and causes clinical bleeding.”
It also serves as a plasma carrier for factor VIII, the antihemophilic factor that facilitates coagulation.

Metabolic and Inflammatory Disorders: There are a number of metabolic or inflammatory disorders that may mimic SBS or that may play a roll in reducing the bodies ability to properly autoregulate after a head injury.

Disorders such as Waldenstrom’s Macroglobulinemia, Multiple Mylomas and Cryoglobulinemia increase a patient’s vulnerability to a head trauma by increasing blood viscosity which impairs blood flow through the capillaries. These disorders have also been known to cause retinal hemorrhages, CNS dysfunction and skin necrosis.

GA-1 is ametabolic disorder which mimics Shaken Baby Syndrome by thinning vein walls and causing spontaneous intracranial or retinal hemorrhages.

Sepsis or Endotoxic Shock Endotoxins are a gram negative bacteria produced when our immune system is put under stress. Illness, stress, antibiotics and vaccines all increase the production of endotoxins in our system. Endotoxins create and/or exacerbate clotting disorders and coagulopathies by binding to the protein walls of the cell and breaking down the endothelium.

Vaccines are counter-indicated for people with coagulation disorders, people with current illnesses and people with fragile immune systems. They are also contraindicated for people with seizures, subdurals, and for premature babies. The research thus far seems to indicate the mechanisms are not so sinister, or complicated. The vaccines exacerbate rebleeds in asymptomatic babies. This is evidenced by the varying ages of blood found in so many of these babies.

When doctors or experts are questioned as to whether a supposed SBS case could be the result of a vaccine injury, they generally indicate that the most common and most severe reaction to vaccines is redness at the site of injection. In fact, studies done by the vaccine companies themselves, admit that it is relatively rare to see redness at the site of injection, but far more common to see systemic reactions to vaccines. Prosecutors argue, even if the vaccines increases the amount of systemic reactions in children; this fact precipitates and instigates shaking rather than serving as an alternative explanation for the subdural hematomas.

Studies done on Hepatitis B RECOMBIVAX HB indicates that out of 432 doses administered to 147 infants, only 0.2% of the infants showed redness at the site of injection, whereas 10.4% had systemic reactions including irritability, fever, diarrhea, fatigue/weakness, diminished appetite and rhinitis (Product insert RECOMBIVAX HB) Merck and Co).
Product inserts from Prevnar, the new adjuvant vaccine made to replace the older and more dangerous form of DPT, lists adverse side effects to the vaccine that run an uncanny resemblance to those seen in the in the medical histories given hours or days prior to the deaths of many of the supposed “shaken babies.”

Antibiotics: Certain antibiotics have been known to increase endotoxins or inhibit coagulation.

Tylenol: The effects of Tylenol and other analgesics have not been thoroughly explored. But, any drug that alters blood viscosity, should be used sparingly when a child has signs of increased intracranial pressure.

References

1 Plunkett (2001). Fatal pediatric head injuries caused by short distance falls. American Journal of Forensic Medicine and Pathology 22, No. 1-12.

2. Reiber, G. (1993). Fatal falls in childhood. The American Journal of Forensic Medicine and Pathology 14(3): 201-207.

3. Root, I. (1992). Head injuries from short falls. The American Journal of Forensic Medicine and Pathology 13(1): 85-87.

4. Howard, M., Bell, B.A. and Uttley, D., (1993). The pathophysiology of infant subdural hematomas British Journal of Neurosurgery, 7, 355-356.

5. Nelson (1996) Nelson Textbook of Pediatrics. 15th ed.

6. Piatt (1999) A Pitfall in the Diagnosis of Child Abuse: External Hydrocephalus, subdural hematomas, and retinal hemorrhages. Neurosurgical Focus 7(4).

7. Lindberg, R. Mechanisms of injury of death: Medicological investigations of death. Spitz and Fisher (1998) 590-636

8. Piatt J., (1999). A pitfall in the Diagnosis of Child Abuse: External Hydrocephalus, Subdural Hematoma & Retinal Hemorrhages. Neurosurgical Focus 7(4)(4):1-9

9. Miller, E. et al (2001). Idiopathic thrombocytopenic purpura and MMR vaccine, Archives of Disease In Children 84:227-229.

10. Harrison (1991) Principles of Internal Medicine. Chapter by Robert Handlin on Disseminated Intravascular Coagulation. 1508-1509.

11. Miller, E. et al (2001). Idiopathic thrombocytopenic purpura and MMR vaccine, Archives of Disease In Children 84:227-229.

http://www.emedicine.com/med/topic2885.htm
Article Last Updated: Nov 16, 2007
AUTHOR AND EDITOR INFORMATION

* Authors and Editors
* Introduction
* Indications
* Relevant Anatomy
* Contraindications
* Workup
* Treatment
* Complications
* Outcome and Prognosis
* Future and Controversies
* Multimedia
* References

Author: Herbert H Engelhard III, MD, PhD, Director, UIC Neuro-Oncology Program, Chief, Division of Neuro-Oncology, Associate Professor, Department of Neurosurgery, University of Illinois at Chicago

Herbert H Engelhard, III, is a member of the following medical societies: American Association for Cancer Research, American Association of Neurological Surgeons, American College of Surgeons, American Medical Association, American Society for Cell Biology, American Society of Clinical Oncology, Chicago Medical Society, Congress of Neurological Surgeons, Illinois State Medical Society, Society for Neuro-Oncology, and Society for Neuroscience

Coauthor(s): Grant P Sinson, MD, Associate Professor, Department of Neurosurgery, Medical College of Wisconsin; G Timothy Reiter, MD, Assistant Professor, Department of Neurosurgery, Penn State College of Medicine; Director, Department of Spinal Neurosurgery and Neurotrauma, Penn State Hershey Medical Center

Editors: Paul L Penar, MD, Professor, Department of Surgery, Division of Neurosurgery, University of Vermont School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc; Herbert H Engelhard III, MD, PhD, Director, UIC Neuro-Oncology Program, Chief, Division of Neuro-Oncology, Associate Professor, Department of Neurosurgery, University of Illinois at Chicago; Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc

Author and Editor Disclosure

Synonyms and related keywords: SDH, subdural hematoma, subdural hemorrhage, acute subdural hematoma, ASDH, subacute subdural hematoma, chronic subdural hematoma, CSDH, intracranial hemorrhage, brain bleed, brain bleeding, contralateral hematoma, subdural hygroma, dementia

INTRODUCTION

A subdural hematoma (SDH) is a common neurosurgical disorder that often requires surgical intervention. SDH is a type of intracranial hemorrhage that occurs beneath the dura and may be associated with other brain injuries. Essentially, it is a collection of blood over the surface of the brain. SDHs are usually caused by trauma but can be spontaneous or caused by a procedure, such as a lumbar puncture. Anticoagulation, such as with heparin or warfarin (Coumadin), may be a contributing factor.

SDHs are usually characterized based on their size, location, and age (ie, whether they are acute, subacute, or chronic). These factors, as well as the neurologic and medical condition of the patient, determine the course of treatment and may also influence the outcome.

SDHs are often classified based on the period that has elapsed from the inciting event (if known) to the diagnosis. When the inciting event is unknown, the appearance of the hematoma on CT scan or MRI can help determine when the hematoma occurred.

Generally, acute SDHs are less than 72 hours old and are hyperdense compared with the brain on CT scan. Subacute SDHs are 3-20 days old and are isodense or hypodense compared with the brain. Chronic SDHs are 21 days (3 wk) or older and are hypodense compared with the brain. However, SDHs may be mixed in nature, such as when acute bleeding has occurred into a chronic SDH.

For the most part, this review discusses acute and chronic SDHs; less information is available about the less common subacute SDHs.1 The entity of subdural hygroma is briefly addressed with chronic SDH.

Acute SDH is commonly associated with extensive primary brain injury. In one study, 82% of comatose patients with acute SDH had parenchymal contusions.2 The severity of the diffuse parenchymal injury correlates strongly (inverse correlation) with the outcome of the patient. In recognition of this fact, an SDH that is not associated with an underlying brain injury is sometimes termed a simple or pure SDH, whereas the term complicated has been applied to SDHs in which a significant injury of the underlying brain has also been identified.

Chronic SDH is a common treatable cause of dementia. Some chronic SDHs may be derived from subdural hygromas. The presence of brain atrophy or loss of brain tissue due to any cause, such as old age, alcoholism, hydrocephalus, or stroke, may provide either an increased space between the dura and the brain surface where a subdural hygroma can form (see Image 6) or traction on bridging veins that span the gap between the cortical surface and dura or venous sinuses. Hygromas probably form after a tear in the arachnoid allows cerebrospinal fluid (CSF) to collect in the subdural space. A subdural hygroma may therefore also occur after head trauma; they are frequently asymptomatic. A minority of chronic SDH cases are derived from acute SDH cases that have matured (ie, liquified) because of lack of treatment.
History of the Procedure

The practice of trephination of the head (ie, chipping or drilling a hole through the skull) has been traced back to ancient times. The author Balzac, in 1840, described a case of chronic SDH, including its traumatic origin and surgical treatment.3 In the late 19th century, with the rise of medicine, development of aseptic technique and anesthesia, and establishment of the basic principles of neurologic localization, surgery for intracranial lesions (including SDH) became more common and, later, survival rates improved. In 1883, Hulke first described successful neurosurgical treatment of chronic SDH.4 Although cerebral angiography could be used to localize SDH in the early–to–mid-20th century, the development of the CT scan in the late 1970s represented another leap in patient care.
Problem

Traumatic injury of the head continues to be a significant health problem in the United States and elsewhere. SDH is the most common type of intracranial mass lesion, occurring not only in patients with severe head injury, but also in patients with less severe head injuries, particularly those who are elderly or who are receiving anticoagulants. SDH can be associated with high mortality and morbidity rates, even with the best medical and neurosurgical care.
Frequency

Acute SDHs have been reported to occur in 5-25% of patients with severe head injuries, depending on the study. Chronic SDH has been reported to be 1-5.3 cases per 100,000 people per year. More recent studies have shown a higher incidence, probably because of better imaging techniques.

Etiology

* Acute SDH
*
o Head trauma
o Coagulopathy or medical anticoagulation (eg, warfarin [Coumadin], heparin, hemophilia, liver disease, thrombocytopenia)
o Nontraumatic intracranial hemorrhage due to cerebral aneurysm, arteriovenous malformation, or tumor (meningioma or dural metastases)
o Postsurgical (craniotomy, CSF shunting)
o Intracranial hypotension (eg, after lumbar puncture, lumbar CSF leak, lumboperitoneal shunt, spinal epidural anesthesia5
o Child abuse or shaken baby syndrome (in the pediatric age group)
o Spontaneous or unknown (rare)
* Chronic SDH
*
o Head trauma (may be relatively mild, eg, in older individuals with cerebral atrophy)
o Acute SDH, with or without surgical intervention
o Spontaneous or idiopathic

Risk factors for chronic SDH include chronic alcoholism, epilepsy, coagulopathy, arachnoid cysts, anticoagulant therapy (including aspirin), cardiovascular disease (hypertension, arteriosclerosis), thrombocytopenia, and diabetes. In younger patients, alcoholism, thrombocytopenia, coagulation disorders, and oral anticoagulant therapy have been found to be more prevalent. Arachnoid cysts are more commonly associated with patients younger than 40 years with chronic SDH. In older patients, cardiovascular disease and arterial hypertension are found to be more prevalent. In one study, 16% of patients with chronic SDH were on aspirin therapy. Major dehydration is a less commonly associated condition and is found concurrently in only 2% of patients.
Pathophysiology

Acute subdural hematoma

The usual mechanism that produces an acute SDH is high-speed impact to the skull. This causes brain tissue to accelerate or decelerate relative to the fixed dural structures, tearing blood vessels, especially bridging veins. The primary head injury may also cause associated brain hematomas or contusions, subarachnoid hemorrhage, and diffuse axonal injury. Secondary brain injuries may include edema, infarction, secondary hemorrhage, and brain herniation.

Often, the torn blood vessel is a vein that connects the cortical surface of the brain to a dural sinus (termed a bridging vein). Alternatively, a cortical vessel, either a vein or small artery, can be damaged by direct injury or laceration. An acute SDH due to a ruptured cortical artery may be associated with only minor head injury, possibly without an associated cerebral contusion. In one study, the ruptured cortical arteries were found to be located around the sylvian fissure.6

In elderly persons, the bridging veins may already be stretched because of brain atrophy (shrinkage that occurs with age).

Like other masses that expand within the skull, SDHs may become lethal by increasing pressure within the brain, leading to pathologic shifts of brain tissue (brain herniations). Two common types of brain herniation include subfalcial (cingulate gyrus) herniation and transtentorial (uncal) herniation. Subfalcial herniation may cause a cerebral infarct via compression of the anterior cerebral artery, and transtentorial herniation may cause an infarct via compression of the posterior cerebral artery. Transtentorial herniation is also associated with pressure on the third cranial nerve, causing decreased reactivity and then dilatation of the ipsilateral pupil.

With progressive transtentorial herniation, pressure on the brainstem causes its downward migration. This tears critical blood vessels that supply the brainstem, resulting in Duret hemorrhages and death. Increased intracranial pressure (ICP) may also decrease cerebral flood flow, possibly causing ischemia and edema and further increases the ICP, causing a vicious circle of pathophysiologic events.

Chronic subdural hematomas

Chronic SDHs may begin as a subdural hygroma, which begins as a separation in the dura-arachnoid interface, which is then filled by CSF. Dural border cells proliferate around this CSF collection to produce a neomembrane. Fragile new vessels then grow into the membrane. These vessels can hemorrhage and become the source of blood into the space, resulting in the growth of the chronic SDH.

Chronic SDHs may also evolve from the liquefaction of an acute SDH, particularly one that is relatively asymptomatic. Liquefaction usually occurs after 1-3 weeks, with the hematoma appearing hypodense on a CT scan.

Chronic SDHs that form from acute SDHs may have membranes between the dura and hematoma at 1 week and between the brain and hematoma at 3 weeks. As stated above, new fragile vessels may grow into these membranes. If not resorbed, the vessels in the membranes that surround the hematoma can hemorrhage repeatedly, enlarging the hematoma. Some chronic SDHs may also enlarge from an osmotic gradient, drawing more fluid into the subdural space, or through the separate mechanism of calcification (Atkinson, 2003).

In 1989, Kawakami discovered that the coagulation and fibrinolysis systems were both excessively activated in chronic SDH.7 This results in defective clot formation and recurrent hemorrhage. Katano et al (2006) recently reported on the status of other molecular markers within chronic SDHs.8
Clinical

Acute subdural hematoma

Acute SDHs are most likely to occur after head injury from a fall, motor vehicle accident, or assault. SDH is more common in men than in women, with a male-to-female ratio of approximately 3:1. Patients with SDH should be examined for related injuries (using guidelines established by the American College of Surgeons Committee on Trauma), such as cervical spine fracture, spinal cord injury, or long-bone fractures.

Patients found to have an acute SDH are usually older than other patients with trauma. In one study, the average age of a patient with trauma but without acute SDH was 26 years, while the average age of patients with an acute SDH was 41 years. Therefore, older patients appear to be at greater risk for developing an acute SDH after head injury. This is believed to be due to older patients having more atrophy, which allows more sheer force against bridging veins immediately after impact.

The clinical presentation of a patient with an acute SDH depends on the size of the hematoma and the degree of any associated parenchymal brain injury.

Some symptoms associated with acute SDH include headache, nausea, confusion, personality change, decreased level of consciousness, speech difficulties, other change in mental status, impaired vision or double vision, and weakness. Of course, such symptoms could also be caused by other conditions.

Neurological findings associated with acute SDH may include the following:

* Altered level of consciousness
* A dilated or nonreactive pupil ipsilateral to the hematoma (or earlier: a pupil with a more limited range of reaction)

* Hemiparesis contralateral to the hematoma.

A host of findings could be associated with these, such as brisk or abnormal reflexes, aphasia (usually with a left-sided hematoma), upper-extremity drift, or impairment of cortical sensory function. Less common findings include papilledema and unilateral or bilateral cranial nerve VI palsy. Some of the above may occur later in the clinical course; for instance, coma with a dilated fixed pupil usually indicates unilateral transtentorial herniation. Lack of a finding (eg, papilledema) cannot rule out SDH.

Less commonly, the hemiparesis may be ipsilateral to the hematoma, possibly due to direct parenchymal injury or compression of the cerebral peduncle contralateral to the hematoma against the edge of the tentorium cerebelli (the Kernohan notch phenomenon). Therefore, if the findings are conflicting, the most reliable indicator (by examination) of the side of the hematoma is a dilated or nonreactive pupil, which appears on the same side as the hematoma.

Patients may have a lucid interval after the trauma that causes a SDH. In addition, initial CT scan findings may be negative (ie, delayed intracranial hemorrhage).

Although acute SDHs most often occur over the cerebral hemispheres (convexity), they may also be found between the hemispheres along the falx (interhemispheric SDH), along the tentorium, or in the posterior fossa. Interhemispheric SDHs may be asymptomatic or manifest as headache,9 impaired consciousness, or hemiparesis or monoparesis (more likely to affect the contralateral leg than arm). Interhemispheric subdurals are usually managed conservatively unless neurologic deterioration is found.10

Chronic subdural hematoma

Men also have a higher incidence of chronic SDH. The male-to-female ratio has been reported to be 2:1. Most adults with chronic SDH are older than 50 years, with 2 studies reporting average ages of 68 and 70.5 years.

One quarter to one half of patients with chronic SDH have no identifiable history of head trauma. If a patient does have a history of head trauma, it is usually mild. The average time between the occurrence of the head trauma and the diagnosis of chronic SDH is 4-5 weeks.

Clinical presentation for chronic SDH is often insidious, with symptoms that include decreased level of consciousness, headache, difficulty with gait or balance, cognitive dysfunction or memory loss, motor deficit (eg, hemiparesis), headache, or aphasia. Chronic SDH may have a presentation similar to that of Parkinson disease.11 An acute presentation is also possible, as in the case of a patient who presents with a seizure.

Neurologic examination may demonstrate mental status changes, hemiparesis, papilledema, hyperreflexia or reflex asymmetry, hemianopsia, or third or sixth cranial nerve dysfunction. Such findings may also be associated with other entities. In patients aged 60 years or older, hemiparesis and reflex asymmetry are common presenting signs. In patients younger than 60 years, headache is a common presenting symptom.

Chronic SDHs have been reported to be bilateral in 8.7-32% of cases.

INDICATIONS

The nature and timing of neurosurgical intervention depends on multiple factors, including the size, age, and location of the hematoma and the medical and neurological condition of the patient. Surgery may be urgently required, yet even emergency surgery does not guarantee a satisfactory outcome.

Surgical evacuation via craniotomy is often considered in patients with an acute subdural hematoma (SDH) thicker than 5 mm (as measured with axial CT scanning) who have any neurological signs, such as lethargy or other change in mental status, or a focal neurological deficit. Bullock et al recently reported that "an acute SDH with a thickness greater than 10 mm, or a midline shift greater than 5 mm on computed tomography (CT) scan should be surgically evacuated, regardless of the patient's Glasgow Coma Scale (GCS) score."12

Surgery for chronic SDH may be indicated if the SDH is symptomatic or is producing significant mass effect, as evaluated with diagnostic imaging.

Diagnostic imaging that shows an expanding hematoma may also indicate the need for surgery, even in some patients whose neurological status is near normal.

RELEVANT ANATOMY

As the name implies, the subdural space is under the dura but above the pia-arachnoid that is intimately associated with the cortical surface. Subdural hematomas (SDHs) are usually hemispheric in location, but may occur along the falx, the tentorium, or in the posterior fossa.

A SDH usually forms after the rupture of a bridging vein. These run from the cortical surface to the dura. Bridging veins are most commonly found along the sagittal sinus and around the anterior tip of the temporal lobe. The source of bleeding may or may not be found at the time of surgery.

CONTRAINDICATIONS

Contraindications to surgery are determined on a case-by-case basis, depending on factors that relate to the patient's neurological and medical condition. For example, a patient with a massive subdural hematoma (SDH) may not be a surgical candidate if he or she has concomitant brain death, anticipated severe neurologic damage, coexisting brain lesions (eg, infarction), or a medical condition that contraindicates general anesthesia or surgery (eg, coagulopathy prior to correction). What is known of the patient's and family's beliefs and instructions may play a role in this decision.

At the other end of the spectrum, small acute SDHs thinner than 5 mm on axial CT images without sufficient mass effect to cause midline shift or neurological signs may be able to be observed clinically. MRI may be more sensitive than CT scan in detecting small SDHs. A chronic SDH with minimal or no mass effect on imaging studies and no neurological symptoms or signs except mild headache is often observed with serial scans and may resolve without surgical intervention.

WORKUP

Lab Studies

* Initial blood tests

o To determine if defective coagulation was involved in the formation of the subdural hematoma (SDH) and to guide correction of any coagulation abnormalities, a prothrombin time (PT), activated partial thromboplastin time (aPTT), and a platelet count are typically performed. A bleeding time assessment may reveal platelet dysfunction.
o Routine trauma laboratory studies that aid in the initial patient assessment may include hemoglobin or hematocrit, electrolytes, and a drug and alcohol screening. The drug and alcohol screenings may be important for correlating the neurological examination with the imaging studies.

Imaging Studies

* CT scan of the head (without contrast)

o An emergent head CT scan needs to be performed when an acute SDH is suspected and should be obtained immediately after the patient is stabilized using standard advanced trauma life support (ATLS) guidelines.
o An acute SDH appears on the noncontrast head CT scan as a crescent-shaped hyperdense area between the inner table of the skull and the surface of the cerebral hemisphere (see Image 7). Acute SDHs are usually unilateral.
o A small acute SDH may be difficult to appreciate because of the appearance of the overlying skull. Use of the bone window setting may aid in discrimination.
o An SDH may also be located along the falx (ie, interhemispheric), along the tentorium, or in the posterior fossa. Interhemispheric SDHs are among the findings identified in some abused children. Rarely, a SDH appears –lens shaped (ie, more like an epidural hematoma).
o All or part of an acute SDH may appear hypodense or isodense to brain if the patient’s hematocrit is low, if the clot is hyperacute (eg, <1 hour old), if the subdural space contains active bleeding, if coagulopathy is present, or if the CSF if creating a dilutional effect. Detection of an isodense SDH may require a high index of suspicion; subtle changes in the appearance or position of the cortical sulci may be found. Contrast-enhanced CT or MRI may help to better define the lesion. Interestingly, isodense SDHs may be either hypointense or hyperintense on T2-weighted MRI; this may be a clue to the underlying pathophysiology.13
*

o The characteristic evolution of an SDH appearance on CT scan is as follows: In the first week, the SDH is hyperdense to brain tissue. In the second and third weeks, the SDH appears isodense to brain tissue (see Images 3-4). After the third week, the SDH is hypodense to brain tissue.
o Often, a chronic SDH appears as a heterogeneously dense lesion indicative of recurrent bleeding with a fluid level between the acute (hyperdense) and chronic (hypodense) components of the hematoma (see Image 2).
o On a contrast-enhanced CT scan, the chronic SDH membrane enhances to varying degrees, depending on numerous factors. Sometimes, a contrast-enhanced scan shows evidence of an underlying cause, such as a tumor or vascular lesion (eg, in patients with acute but nontraumatic SDH).
o Typical signs of mass effect, such as midline shift and ventricular compression, may be observed.
* Magnetic resonance imaging

o MRI is less useful than CT in diagnosing an acute SDH because of the increased time needed to obtain the study and the inability to use metallic objects that are needed to resuscitate patients with trauma (eg, most ventilators) in the scanning environment.
o MRI can be a useful study to evaluate associated parenchymal brain injury and predict prognosis, but only after stabilizing and treating any life-threatening lesions. MRI is more sensitive for detecting nonhemorrhagic brain lesions, contusions, and diffuse axonal injury.14
o An MRI is helpful in imaging chronic SDH when CT scans are difficult to interpret (eg, when suspecting an isodense hematoma). MRI may be particularly helpful in diagnosing bilateral chronic SDH because a midline shift may not be apparent on CT scan.

Histologic Findings

Acute SDHs usually contain both liquid and clotted blood. Intact erythrocytes are usually found within the clot. Associated skull fractures and underlying focal traumatic parenchymal damage are often present.

Fibroblastic membranes form on the dural side and arachnoid side of the chronic SDH, with the dural neomembrane being more vascular. The neomembrane consists of many capillaries, intact and lysed erythrocytes, hemosiderin-laden macrophages, and granulation tissue.

TREATMENT

Medical therapy

Acute subdural hematoma

Emergency medical treatment of a patient with an acute subdural hematoma (SDH) that causes impending transtentorial herniation may include bolus administration of mannitol (in patients whose fluid levels have been adequately resuscitated and who have adequate blood pressure). Surgical evacuation of the lesion is the definitive treatment. Hyperventilation might be required but may decrease cerebral blood flow, thereby causing cerebral ischemia.

A patient with coagulopathy or a patient with an acute SDH who is receiving anticoagulant medication should be transfused with fresh frozen plasma (FFP), platelets, or both to maintain the prothrombin time (PT) within the reference range and the platelet count above 100,000. Heparin may need to be reversed with protamine; patients receiving warfarin are given vitamin K. Platelet infusion may also need to be considered if the platelet count is adequate but platelet function is impaired. The use of other factors, such as recombinant factor VII is under investigation. In patients who are receiving therapeutic anticoagulation, the potential effects of reversing the anticoagulation need to be considered.

The use of sequential CT scanning is important. Although each patient must be treated individually, patients who have small acute SDHs thinner than 5 mm on axial CT images without sufficient mass effect to cause midline shift or neurological signs have been observed clinically, with acceptable results (see Image 1). Hematoma resolution should be documented with serial imaging because an acute SDH that is treated conservatively can evolve into a chronic hematoma. For serial imaging, MRI may be more sensitive, but CT may be more convenient and less expensive.

Chronic subdural hematoma

In patients who have no significant mass effect on imaging studies and no neurological symptoms or signs except mild headache, chronic SDHs have been observed with serial scans and have been seen to remain stable or to resolve.

Although hematoma resolution has been reported, it cannot be reliably predicted, and no medical therapy has been shown to be effective in expediting the resolution of acute or chronic SDHs.
Surgical therapy

Acute subdural hematoma

Surgery to manage an acute SDH usually consists of a large craniotomy (centered over the thickest portion of the clot) to decompress the brain, to stop any active subdural bleeding, and if indicated, to evacuate intraparenchymal hematoma in the immediate vicinity of the acute SDH. An acute SDH usually has a consistency that is too firm to allow removal through burr holes alone.

Including the sylvian fissure in the craniotomy exposure should be considered, since this is a likely location of a ruptured cortical vessel. If brain injury and edema are associated with the SDH, an ICP monitor may need to be placed. Bullock and colleagues (2006) stated that "all patients with acute SDH in coma (Glasgow coma scale [GCS] score less than 9) should undergo intracranial pressure monitoring."12 Craniectomy (ie, the removal of the bone plate or flap) is also sometimes required, such as when increased ICP is present or anticipated. Different methods for storing the bone flap for possible later replacement exist.

Chronic subdural hematoma

Various surgical techniques for the treatment of chronic SDH have been described. Liquefied chronic SDHs are commonly treated with drainage through 1 or 2 burr holes. The burr holes are placed so that conversion to a craniotomy is possible, if needed. A closed drainage system is sometimes left in the subdural space for 24-72 hours postoperatively. Drainage via twist-drill craniotomy at the bedside has also been described.15, 16 Recently, a new system, the Subdural Evacuating Port System, has been introduced, with encouraging results.17

Under certain circumstances, craniotomy is recommended for chronic SDH, depending on factors such as recurrence, the consistency of the hematoma, and the presence of membranes.

Bilateral chronic hematomas may require drainage from both sides, usually during the same operation by means of burr holes placed on each side of the head.
Preoperative details

Phenytoin (Dilantin) is administered to decrease the risk of developing early posttraumatic seizures (within the first 7 d after the injury). Patients have an estimated risk of greater than 20% for developing posttraumatic epilepsy after an acute SDH. Whether this risk is modifiable with prophylactic anticonvulsants remains debatable.
Intraoperative details

The surgical technique for removing an acute SDH is well described in most standard texts of neurosurgery. When an acute SDH is evacuated, intraoperative ultrasonography may be helpful for locating intraparenchymal clots, which also may require evacuation, depending on the risks and benefits involved. Perioperative antibiotics may be administered to decrease the risk of postoperative infection.
Postoperative details

Acute subdural hematoma

After the evacuation of an acute SDH, medical treatment is aimed at controlling the ICP below 20 mm Hg and maintaining the cerebral perfusion pressure above 60-70 mm Hg.

A follow-up CT scan is usually obtained within 24 hours of acute SDH removal and as needed to monitor for residual hematoma and recurrence.

If elevated ICP is an issue postoperatively, an urgent CT scan should be obtained to look for a new intracranial mass lesion or reaccumulation of the SDH.

Postoperative coagulation studies (PT, aPTT) and platelet counts should be observed closely and adjustments made, when possible, to lessen the risk of additional bleeding.

Chronic subdural hematoma

After the evacuation of a chronic SDH, adequate patient hydration is needed to help reexpand the brain. In addition, the patient may be maintained on bedrest with the head of the bed flat to aid brain reexpansion by increasing the intracranial venous pressure.
Follow-up

Acute subdural hematoma

Serial neurological examinations are used to determine the patient's subsequent clinical course (whether the patient is stable, improving, or deteriorating). Coagulation tests (PT, aPTT) and platelet counts may need to be observed and adjustments made in certain patients in order to decrease the risk of rebleeding.

Depending on the severity of the neurologic injury, patients may require physical therapy, occupational therapy, long-term rehabilitation, or even nursing-home placement.

Although CT imaging alone is usually sufficient for short-term management, a brain MRI is sometimes used (after a patient is stabilized) to look for associated brain injuries.

Serial imaging studies may be necessary to confirm that the acute SDH has fully resolved; a residual hematoma could become a symptomatic chronic SDH. This transformation can occur regardless of whether the hematoma has been managed surgically or conservatively.

Chronic subdural hematoma

As with acute SDH, serial neurological examinations are used and coagulation parameters may need to be followed. Serial CT scans are used to document the resolution of the chronic SDH.

Depending on the patient, physical therapy, occupational therapy, long-term rehabilitation, or even nursing home placement may be needed.

If the patient was on anticoagulation therapy preoperatively, when to restart anticoagulation therapy is complicated. No solution is perfect. The risks and benefits of anticoagulation must be weighed against the risks of rebleeding to determine when to restart therapy.

COMPLICATIONS

Acute subdural hematoma

As mentioned above, parenchymal brain injury is commonly associated with acute subdural hematoma (SDH) and can lead to increased ICP. Residual neurologic problems, as well as secondary events, can result from these associated injuries.

As with every medical condition and treatment, inherent risks exist. Postoperatively, recurrent or residual hematoma might be present, which, if symptomatic, may require repeat operative intervention. As many as one third of patients experience posttraumatic seizures after a severe head injury. Wound infection and CSF leak are possible after craniotomy. Meningitis or cerebral abscess can occur after any intracranial procedure, and constitutional signs of infection, delayed neurological deterioration, or signs of meningeal irritation may require further evaluation.

A long list of potential complications may also be related to anesthesia and hospitalization.

Chronic subdural hematoma

Among patients with chronic SDH who underwent surgical drainage, 5.4-19% experienced medical or surgical complications. Medical complications, including seizures, pneumonia, empyema, and other infections, occurred in 16.9% of cases. Surgical complications, including acute SDH formation, intraparenchymal hematoma, or tension pneumocephalus, occurred in 2.3% of cases.

After surgery for SDH, even with normalization of ICP, a persistent space may exist between the brain and dura, since the brain may not expand to fill this space. Residual hematoma has been found on 92% of postoperative CT scans within 4 days of operation; however, clinical improvement may proceed regardless of the size of this collection.

Reoperation rates for reaccumulation of hematoma have been reported to be from 12-22%. When the reoperation for burr-hole drainage was compared with craniotomy drainage, similar rates of 18.5% and 12.5% were found. However, the total number of craniotomies performed in this series was small. Of the patients who require a second operation to drain a reaccumulated hematoma, 26.6% (a total of 4 patients) required a third procedure to drain reaccumulated hematoma. Two of these 4 patients who underwent 3 operations developed subdural empyema. In another series, contralateral hematomas formed in 4% of patients who underwent drainage of unilateral chronic SDHs. These occurred from 3 days to 6 weeks postoperatively.18

Postoperative seizures have been reported in 3-10% of patients. Whether prophylactic anticonvulsants therapy can decrease this risk is debatable. Subdural empyema, brain abscess, and meningitis have been reported to occur in less than 1% of patients after operative drainage of a chronic SDH. In these patients, numerous potential complications are also related to anesthesia, hospitalization, patient age, and concurrent medical conditions.

OUTCOME AND PROGNOSIS

Acute subdural hematoma

The mortality rate of acute subdural hematoma (SDH) has been reported to range from 36-79%. Many survivors do not regain previous levels of functioning, especially after an acute SDH severe enough to require surgical drainage. Favorable outcome rates after acute SDH range from 14-40%.

Several series have shown an increase in favorable outcome in younger patients.19 Ages younger than 40 years were associated with a mortality rate of 20%, whereas ages of 40-80 years were associated with a mortality rate of 65%. Ages older than 80 years carried a mortality rate of 88%.

Findings demonstrated by CT scan (or MRI) may help indicate prognosis. Such findings may include the thickness or volume of the hematoma, the degree of midline shift, the presence of associated traumatic intradural lesions, and the compression of the brainstem or basal cisterns.20 The first CT scan may underestimate the size of parenchymal contusions.

Elevated ICP postoperatively indicates a poor prognosis and may indicate the severity of the underlying brain injury (eg, trauma, secondary infarction).

In general, a poor preoperative neurologic status may be a harbinger of a poor outcome. In addition to factors discussed above, poor prognostic indicators for acute SDH have been reported to include the initial and postresuscitation Glasgow coma scale (GCS), the GCS motor score on admission, pupillary abnormalities, alcohol use, injury by motorcycle, ischemic damage,21 hypoxia or hypotension, and overall ability to control ICP.22, 23, 20

Regarding surgical timing, the adage "the sooner the surgery is done, the better" may not always be accurate. This is for various reasons and depends on the individual case.23 Even 15 years ago, Wilberger and colleagues concluded that "the time from injury to operative evacuation of the acute SDH in regard to outcome morbidity and mortality was not statistically significant when examined at hourly intervals".22 However, in patients with acute SDH and indications for surgery, surgical evacuation should be performed as soon as possible.12

Chronic subdural hematoma

Outcome after drainage of a chronic SDH has also been found to correlate with preoperative neurologic status (see Image 5). Early diagnosis before a significant neurologic deterioration may correlate with a more favorable prognosis. No correlation has been found between preoperative CT scan findings and postoperative outcome.

The mortality rate within 30 days of surgery is 3.2-6.5%. Eighty percent of patients resume their prehematoma level of function. Sixty-one percent of patients aged 60 years or younger and in 76% of patients older than 60 years have favorable outcomes. In a relatively recent series, 89.4% of patients with chronic SDH who were treated with a closed drainage system had a good recovery and 2.2% worsened.24 Mori et al found that old age, pre-existing cerebral infarction, and subdural air after surgery correlated with poor brain expansion.25 Stanisic et al (2005) reported a 14.9% postoperative recurrence rate; various factors were associated with this.25

The nature and timing of neurosurgical intervention depends on multiple factors, including the size, age, and location of the hematoma and the medical and neurological condition of the patient. Surgery may be urgently required, yet even emergency surgery does not guarantee a satisfactory outcome.

Surgery for chronic SDH may be indicated if the SDH is symptomatic or is producing significant mass effect, as evaluated with diagnostic imaging.

Diagnostic imaging that shows an expanding hematoma may also indicate the need for surgery, even in some patients whose neurological status is near normal.

Medical therapy

Acute subdural hematoma

Chronic subdural hematoma

Acute subdural hematoma

Chronic subdural hematoma

Under certain circumstances, craniotomy is recommended for chronic SDH, depending on factors such as recurrence, the consistency of the hematoma, and the presence of membranes.

Bilateral chronic hematomas may require drainage from both sides, usually during the same operation by means of burr holes placed on each side of the head.
Preoperative details

Acute subdural hematoma

After the evacuation of an acute SDH, medical treatment is aimed at controlling the ICP below 20 mm Hg and maintaining the cerebral perfusion pressure above 60-70 mm Hg.

A follow-up CT scan is usually obtained within 24 hours of acute SDH removal and as needed to monitor for residual hematoma and recurrence.

If elevated ICP is an issue postoperatively, an urgent CT scan should be obtained to look for a new intracranial mass lesion or reaccumulation of the SDH.

Postoperative coagulation studies (PT, aPTT) and platelet counts should be observed closely and adjustments made, when possible, to lessen the risk of additional bleeding.

Chronic subdural hematoma

Acute subdural hematoma

Depending on the severity of the neurologic injury, patients may require physical therapy, occupational therapy, long-term rehabilitation, or even nursing-home placement.

Although CT imaging alone is usually sufficient for short-term management, a brain MRI is sometimes used (after a patient is stabilized) to look for associated brain injuries.

Chronic subdural hematoma

As with acute SDH, serial neurological examinations are used and coagulation parameters may need to be followed. Serial CT scans are used to document the resolution of the chronic SDH.

Depending on the patient, physical therapy, occupational therapy, long-term rehabilitation, or even nursing home placement may be needed.

Acute subdural hematoma

A long list of potential complications may also be related to anesthesia and hospitalization.

Chronic subdural hematoma

Acute subdural hematoma

Elevated ICP postoperatively indicates a poor prognosis and may indicate the severity of the underlying brain injury (eg, trauma, secondary infarction).

Chronic subdural hematoma

Although surgical intervention may be able to successfully remove the hematoma itself, patients with acute subdural hematomas (SDHs) are often difficult to treat and may have a poor outcome due to underlying brain injury. The medical issues, especially in older patients with SDH, may be complex.

The mechanism, exact pathophysiology, and optimal treatment for chronic SDH has still not been definitively determined. Further work in delineating why membranes form and how to prevent or reverse their formation may lead to improvements in treatment strategies.

Future studies of patients with brain injuries, including those who have SDH, will hopefully lead to improved strategies for prevention of secondary injury and improved recovery from the primary brain injury.

http://tinyurl.com/apv3vx

Premature and Congenitally Diseased Infants
by Julius H. Hess, M.D.
Chapter XIII
Diseases of the Nervous System

Non-traumatic Cerebral Hemorrhage

"In our experience mental disturbances and defects on the part of the central nervous system have been confined largely to those infants who survived from among the class of so-called weaklings. These are the infants who have suffered from intra-uterine disease or congenital malformations, traumata at birth, or postpartum dietetic errors and infection. Among the more mature that are normal for their fetal age the prognosis for a full mental development is good.

Treatment. -- In the postmortem examination of infants dying of cerebral hemorrhage, Rodda [1] found over 50 per cent followed non-instrumental deliveries and many followed normal and easy births. In these cases the blood was found slightly or not at all coagulated. Cerebral hemorrhage was by far the most frequent cause of death in the newborn in his group of cases. In many cases at postmortem, no torn veins were found in the cerebrum or cerebellum to account for the hemorrhage, and multiple hemorrhages were found in portions of the body where it was inconceivable that they could be explained by trauma. Over 25 per cent of all infants dying of cerebral hemorrhage showed this picture of multiple hemorrhages. An analysis of cases reported in the literature deepened the conclusion that these hemorrhages were due to factors other than trauma. Further study led to the conclusion that there was a disturbance in the coagulation time of the blood in the new born. It was found that the average coagulation time in the new born was seven minutes. In icterus, melena, jaundice, syphilis and non-traumatic cerebral hemorrhage, the coagulation time of the blood was prolonged. In melena it might be delayed to ninety minutes. The subcutaneous injection of normal blood was effective in cases in which there was delayed or slow bleeding.

The further treatment in those cases with a diagnosis of intracranial hemorrhage is symptomatic and expectant. There is always the possibility that there may be spontaneous cure. The infant must be kept quiet and warm. For the motor hyperirritability and convulsions narcotics may be employed, before all chloral hydrate (0.12 to 0.5 gm per day per rectum), also bromides (0.25 to 1 gm. per day) or calcium lactate (1 to 2 gm.) or calcium bromide (0.3 to 0.5 gm. per mouth) per day."

http://www.newscientist.com/article/mg20126931.800-the-
pathologist-challenging-shaken-baby-syndrome.html?full=true

Dr. Irene Scheimberg, Pathologist: (Interview)

Non-Traumatic Subdural Hematoma

"The problem with the shaken baby controversy is that it's very dogmatic. If I don't accept religious dogma (and I don't), I'm not going to accept scientific dogma. If it's there, it can be proven. I do recognise that some adults are capable of doing nasty things to children, but I'm uneasy about people saying: "Oh, if a baby has got subdural haemorrhage (SDH), retinal haemorrhage and brain swelling, it can only be shaken baby syndrome." I'm trying to find out the mechanism of bleeding in the brain in babies who have not been shaken.

Have you any clues as to what the mechanism causing "shaken baby" symptoms might be?

I'm exploring all sorts of theories. My colleague Marta Cohen from Sheffield Children's Hospital and I have just published a paper with observations of our autopsy work on fetuses and babies over the last couple of years. We selected 55 cases - 25 late third trimester fetuses who died shortly before delivery and 30 newborns - who had haemorrhage within the membrane that covers and separates the two halves of the brain, and compared this with the level of brain hypoxia, or oxygen deficiency. We knew that none of these cases could possibly be inflicted trauma. We found that all those with severe brain hypoxia and half of those with moderate brain hypoxia had SDH. This is the same type of SDH that some people describe as specifically indicative of shaken baby syndrome. A similar pattern of haemorrhages has been described in the retinas of newborn babies dying of natural causes. We think that in these cases the haemorrhaging is caused by the hypoxia.

My concern is that by relying on this famous triad of symptoms - brain hypoxia, SDH and retinal haemorrhages - to diagnose shaken baby syndrome, when there's no evidence of inflicted trauma, we may be sending to jail parents who lost their children through no fault of their own. As scientists it's our duty to be cautious when we see the triad, and to take each case on its merits. We owe it to the children and their families."

http://www.ncbi.nlm.nih.gov/pubmed/7143728?dopt=Abstract
Rinsho Ketsueki. 1982 Aug;23(8):1235-40.
[A case of scurvy with subdural hematoma] (Japanese article)
Miura T, Tanaka H, Yoshinari M, Tokunaga A, Koto S, Saito K, Izumi J, Inagaki M.

http://tinyurl.com/csxm5y
[Scurvy--a mistakenly forgotten disease]
[Article in German]
Hürlimann R, Salomon F.
Departement für Innere Medizin, Universitätsspital Zürich.

Four cases of scurvy diagnosed within a period of two years are reported. They comprised 2 male patients with heavy nicotine and alcohol abuse, a 35-year-old woman with malnutrition due to food supplements phobia, and a 69-year-old woman with malnutrition due to dementia and social isolation. All four patients were adynamic and anemic. Three patients showed typical dermatologic signs with hemorrhagic hyperceratosis, suffusions or cork-screw hair. Two patients complained of parodontol disorders. Other symptoms were gastrointestinal bleeding, sicca syndrome, retinal bleeding, subdural hematoma, edema and arthralgia. Associated disorders were folic acid and vitamin B12 depletion in two cases, and nephropathy and pneumonia with pneumothorax in one case each. In all cases the serum asorbic acid concentration was below the scorbutic level of 11 mumol/l. Historical data, pathogenesis, incidence, clinical presentation, diagnosis and therapy of scurvy are discussed. We conclude that scurvy can be observed even in a developed country such as Switzerland at the end of the 20th century. The real incidence may be underestimated because symptoms are not well known and disappear rapidly after admission because of sufficient vitamin C content in normal diet. Patients at risk are socially isolated alcoholics, old people, psychiatric patients and diet enthusiasts. Usually scurvy occurs in conjunction with other deficiencies. Smoking and acute illness enhance ascorbic acid depletion. With a knowledge of the symptomatology of scurvy, it is easy to diagnose and treatment is simple and effective. PMID: 8091164 [PubMed - indexed for MEDLINE]

following science or medical journal abstracts, certain assumptions are made. "Comparison of accidental and nonaccidental traumatic injury...." But how did they determine which cases were accidental and nonaccidental? It's very simple. If there was documented evidence of accidental injury, they join the "accidental" group. If there is no documented evidence of an accident, they are assumed to be nonaccidental. How many of these cases have "documentation" of anything? Very few. That would mean they were videotaped, observed by objective unrelated witnesses, or incidents like vehicle or playground accidents. No proof, then the symptoms are considered to be inflicted, which means there is no scientific basis to support the studies comparing the two types of injuries. Even worse, this assumes head impact and ignores the usual lack of any sign of external trauma, when there may have been medical causes.

PHOTOS AND REFERENCES

http://emedicine.medscape.com/article/413463-overview

INFANTS

Mortality/Morbidity

* Scurvy can lead to many other conditions, such as mental status alteration, gum disease and tooth loss, ecchymoses, hemarthrosis, the failure of wounds to heal, the breakdown of healed ulcers, heart and skeletal muscle damage, abruptio placentae, gastrointestinal blood loss, and arrested skeletal development.
* Epiphyseal separation at the epiphyseal plate is a complication.
* Sudden death has been reported.

Sex
Males and females are equally affected.

Age
Those most commonly affected are children aged 6-18 months; however, adults can also be affected. Unless the mother had a deficiency herself, the maternal contribution of vitamin C is generally protective of infants younger than 6 months.
Presentation

Presentation and natural history

Perivascular hemorrhage and lifting of the periosteum caused by hemorrhage are the main anatomic alterations depicted on radiographs. This hemorrhage is due to increased capillary fragility. In scurvy, there is normal mineralization of osteoids; however, the overall amount is decreased. This process is distinct from that in rickets, in which the lack of vitamin D results in defective mineralization of a normal organic matrix.

Scurvy is the direct result of vitamin C deficiency. Vitamin C is required for prolyl and lysyl hydroxylase activity and is essential for collagen synthesis. Defective collagen compromises skin, joint, bone, and vascular integrity. Vitamin C is also required for carnitine synthesis, and it is critical for fatty acid transportation into the mitochondria. This oxidative metabolism is also critical for muscle function.

Scurvy is usually caused by a lack of dietary vitamin C related to inadequate food intake, the destruction of vitamin C in food caused by cooking and canning, or the absence of fresh fruit in the diet. Malabsorption, tobacco use, chronic oxidative stress (eg, HIV infection, inflammatory bowel disease, endotoxemia, diabetes, heat stress), hemodialysis, and therapy with the folic acid antagonist aminopterin all reduce the level of vitamin C in the body. In studies of vitamin C deficiency, the most common associated causes included poor dentition, gastrointestinal disease, food fads, and alcoholism.6,7
The normal total-body pool of vitamin C is 1500 mg. The normal plasma level of vitamin C is 0.7-1.2 mg/dL. Scurvy occurs when the total-body vitamin C level is below 350 mg. The elimination of vitamin C from the diet results in scurvy within 2-3 months. A total vitamin C intake of 10 mg/d maintains the total-body pool above 350 mg and prevents scurvy.

Clinical symptoms include the following:

* Lethargy, listlessness, mental confusion, and fatigue
* Pale, bloated complexion and dry, rough skin as a result of defective collagen
* Hair follicle enlargement and plugging; perifollicular congestion; proliferation of blood vessels; formation of lumps in hair follicles; fractured, coiled, or bent hairs; and perifollicular hemorrhage caused by defective collagen
* Swollen and purple gums, putrid and bleeding gums, or loosened teeth as a result of defective collagen
* Ecchymoses due to blood-vessel fragility (Purpura may become palpable.)
* Costochondral junction swelling; hemarthrosis; and pain, stiffness, or swelling of the knees or ankles as a result of bleeding
* Arrested skeletal development caused by defective collagen
* Impaired wound healing and breakdown of previously healed ulcers caused by defective collagen
* Dyspnea, chest pain, abruptio placentae, intraocular hemorrhage, diarrhea, and gastrointestinal blood loss caused by fragile blood vessels and defective collagen
* Femoral nerve compression by hematomas
* Normocytic anemia and macrocytic anemia related to osmotic fragility of the red blood cells
* Hypotension due to blood loss and vascular fragility
* Hematuria
* Subdural hemorrhage
* Sudden death

this is further compounded by the fact that the use of vitamin C supplements may lead to oxalosis, which can cause renal and liver problems. Often, physicians have avoided vitamin supplementation in order to safeguard against oxalosis. New research suggests that the benefits of vitamin C supplementation and advances in dialysis techniques may lead to an increased use of vitamin C to control anemia for dialysis patients.8

Dianne Jacobs Thompson Est. 2007
Also http://truthquest2.com (alternative medicine featuring drugless cancer treatments)
Author publication: NEXUS MAGAZINE "Seawater--A Safe Blood Plasma Substitute?"