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.
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, 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.
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.
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.