Next to blood, the most important tissue for toxicological purposes is vitreous. In some ways, vitreous has an advantage over blood in that, caused by its acellular nature and relative isolation, it is less susceptible to biochemical changes and contamination. Because of this, valid electrolyte studies can be done on the vitreous that cannot be performed on blood. In the case of certain drugs, such as alcohol, vitreous can provide a picture of the blood concentration 1-2 h prior to death. Unlike spinal fluid, vitreous is also easy to obtain.

Analysis of postmortem blood for concentrations of sodium, potassium, and chloride give erroneous results. Sodium and chloride decrease in the blood after death, while potassium increases, due to breakdown of cells. Thus, one cannot use postmortem blood to accurately determine an individual's electrolyte status immediately prior to death. Fortunately, electrolyte abnormalities in living individuals are often reflected in the vitreous. Because vitreous levels of sodium and chloride are valid, this makes diagnosis of antemortem electrolyte imbalances possible. Unfortunately, this does not hold true for vitreous potassium.

The normal levels of sodium and chloride in vitreous are 135 to 151 meq/L and 105-132 meq/L, respectively, if significant cellular and tissue breakdown (decomposition) has not set in.33 Decomposition of a body is reflected in the vitreous by a potassium level of 15 meq/L or above. When potassium is 15 meq/L or greater, the sodium and chloride values fall, making electrolyte evaluation of questionable value.34

If potassium values are less than 15 meq/L, then sodium values below 135 meq/L and chloride values below 105 meq/L indicate that one is dealing with low salt syndrome. This is seen most commonly in association with severe fatty metamorphosis of the liver or micronodular cirrhosis. Coe described six cases of profound salt depletion. In one case, sodium was106 meq/L; chloride 87 meq/L, and potassium 6.2 meq/L due to prolonged use of diuretic therapy.35 The same picture of a low salt syndrome can be caused by overhydration, or water intoxication. In a fatal case of water intoxication seen by one of the authors, vitreous sodium was 115 meq/L, chloride 105 meq/L, and potassium 7.6 meq/L.32 In individuals with dehydration, sodium is greater than 155 meq/L, chloride greater than 135 meq/L, and urea greater than 40 mg/dL. In uremia, sodium and chloride are usually within normal limits, with vitreous urea usually greater than 150 mg/dL.35

Vitreous potassium levels are of no help in determining what the potassium status of an individual was immediately prior to death, because potassium is released almost immediately postmortem, even in the vitreous. Elevated levels of potassium, therefore, have no diagnostic value in the vitreous. Low levels of potassium in the vitreous, indicative of hypokalemia, are valid, but the authors have virtually never seen this, even in cases where the individual is known to be hypokalemic. Attempts have been made to determine the time of death by vitreous potassium levels. Such attempts have been unsatisfactory.

Normal levels of glucose in the vitreous range anywhere from 0 to 180 mg%. Vitreous glucose levels are of significance if elevated, but are of no significance if low. An elevated vitreous glucose is an accurate reflection of an elevated antemortem blood glucose. Glucose levels significantly above 200 mg/dL in the vitreous are considered diagnostic of diabetes mellitus.36

Agonal hyperglycemia is extremely common, especially if there has been attempted resuscitation. It plays no part in contributing to the death, however. Agonal hyperglycemia is not reflected in the vitreous. Thus, Coe reported that, in all of 102 nondiabetics in whom postmortem peripheral blood glucose concentration exceeded 500 mg/dL from a terminal rise in blood sugar, the vitreous glucose was below 100 mg/dL.37 Even if intravenous glucose infusions are administered prior to death, the vitreous glucose levels in normal subjects are generally less than 200 mg/dL.

In individuals with elevated levels of glucose in the vitreous due to hyperglycemia, there is a gradual fall in vitreous levels postmortem. The fall is gradual enough to allow diagnosis of hyperglycemia for a considerable time after death. Unfortunately, because normal individuals start at significantly lower levels of vitreous glucose, the decline is sufficiently rapid that low levels of glucose are the rule. Because of this, one cannot differentiate a low vitreous glucose level caused by hypogycemia from that of normal postmortem decline in an indiviual who had a normal glucose level at the time of death. Thus, perfectly normal individuals who die of trauma might be found to have a vitreous glucose level of 0 or 5 mg/dL, which is obviously an artifactual phenomenon.

Vitreous bilirubin is of no value diagnostically, with normal values in jaundiced individuals who have antemortem serum levels of greater than 30 mg/dL.33 Values for alkaline phosphatase, SGOT, and calcium are also of no value. Vitreous urea, however, is valuable for diagnostic purposes. Its normal range is within the same normal range as blood urea nitrogen. It is the most stable component of vitreous. Blood urea nitrogen levels postmortem are also valid over prolonged time. Creatinine determinations are valid in both vitreous and blood.

Because of the work of Dr. John Coe, the importance of vitreous as an agent in postmortem chemistry has been realized.33-35,37 What still is not fully appreciated is that vitreous can also be of great value in drug identification and interpretation. Vitreous alcohol concentrations are often of value in making the diagnosis of death from acute alcohol intoxication occurring in both the absorptive and the nonabsorptive phases. A young boy may present with a fatal blood alcohol level of 0.450 g/dL and a vitreous alcohol of 0.12 g/dL. This indicates that he was ingesting large quantities of alcohol over a short time and died before there could be any equilibration between blood and vitreous. Other individuals take in a large amount of alcohol over a longer period of time, lapse into an irreversible coma due to the central nervous depressant action of the alcohol, and suffer irreversible brain injury, yet still "live" for a significant time after ingestion. In such cases, one may find a vitreous alcohol of 0.400% and a blood alcohol of 0.250%.

In addition to analysis for alcohol, one of the authors (VJMD) has had extensive experience with the use of vitreous for other drug determinations. Thus, cocaine, morphine, propoxyphene, and the tricyclic antidepressants and their metabolites have all been identified in vitreous. The levels of the drugs and metabolites in the vitreous can be used in conjunction with blood levels to make determinations as to the manner of death, because, just like those of alcohol, these levels are a reflection of what the blood levels were an hour or two prior to death. Thus, one can better evaluate the status of how an individual took a drug, whether as an acute overdose, an acute overdose with prolonged survival, or was a chronic abuser of the drug.

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