However, the processes triggered by death and the post-mortem interval The relationship between PMI and RNA stability is very tissue-dependent (Fig. from M.M.A., F.R., J.D., M.S., and K.A. All authors revised the paper. I am thinking of calling Jake for a relationship postmortem I don't think we can be friends again unless I get some closure. Relationship ka postmortem::| ♥ dayline.info READ Girl-"us ladki ko delete kr do. .wo achchi ni hai boy-"ok. kui baat ni.. kr de ra dayline.info
There has been extensive debate on the utility of vitreous potassium as a predictor of PMI [ 203132 ]. For instance, one study found only a slight change in vitreous potassium levels and time since death, but this change was not significant [ 20 ]. However, the authors do state that most studies have found a useful relationship [ 20 ]. Over the years, many scientists have confirmed the existence of this relationship and created different formulas to estimate the time of death with varying accuracy [ 33 - 35 ].
Many of the statistical models and equations derived to estimate time since death are based on the assumption that the post-mortem increase in vitreous potassium is fairly linear with time and changes at a constant rate [ 23 ]. There are studies in the literature reporting a not entirely linear relationship between vitreous potassium and PMI [ 30 ].
Most studies have shown that potassium can be a useful tool in estimating time since death during the early post-mortem period. There however, is no agreement on the duration until when vitreous potassium can be considered a reliable criterion for estimation of time since death. Adjutantis and Coutselinis reported a possibility of accurate prediction of time since death within 2 h from the estimation of potassium in the VH [ 32 ].
Leahy and Farber did not find any mathematical relationship between vitreous potassium and post-mortem interval in cases of sudden death [ 28 ]. Forensic scientists are of the opinion that vitreous potassium should not be the definitive method of choice for estimation of post-mortem interval but used selectively and in conjunction with other tests [ 30 ]. Vitreous potassium levels [ 14 ] are of no help in determining the potassium status of an individual immediately prior to death.
Relationship between sudden natural death and abdominal fat evaluated on postmortem CT scans
Increased vitreous potassium levels have no diagnostic value, whereas low vitreous levels are theoretically indicative of hypokalemia [ 14 ]. The correlation strength between the PMI and the potassium level depends on various factors such as the cause of death, the duration of the agonal episode, and the temperature extrinsic factorsas well as the age, sex, and physiological and pathological state of the deceased intrinsic factors [ 1441 ].
Factors such as age, sex, cause of death, season of death, and refrigeration of sample were found not to influence VH potassium values [ 24 ]. For determining the potassium concentration in the VH, pre-analytical, analytical, and instrumental factors should be taken in consideration [ 17 ].
Unlike other parameters in VH e. It seems that in the initial period after death probably up to 6 hours intensive production of lactates occurs in cytosol [ 294142 ].
In the presently available literature no equation for the estimation of the PMI by use of vitreous lactate is found [ 42 ]. The levels of sodium and chloride were found by others to be relatively stable in the early post-mortem period, and thus may be useful in the determining the mechanism of death [ 26 ].
Studies have shown that the concentration of sodium and chloride fall slowly after death, while potassium slowly rises [ 20 ], these changes are reported to be in proportion to the PMI [ 9303540 ]. However, it was also found that the correlation between vitreous electrolytes and time since death was not statistically significant [ 20 ]. It has been concluded that the sodium, calcium, and chloride levels have no role in estimating PMI [ 23 ].
No age related changes in electrolytes have been found in vitreous electrolytes in several different populations [ 92038 ]. Nevertheless, it has been suggested that the age of an individual may have an effect on vitreous potassium [ 45 ]. It has also been suggested that the rates of potassium may be different in children and that in the case of children, age may play a role [ 46 ].
Although there is considerable literature on hypernatremia in clinical settings, less has been written on the potential significance of this finding after death [ 26 ]. The serum concentration reflects the total body exchangeable sodium relative to water content [ 48 ]. In addition to reduced intake of fluid, hypernatraemia may be a marker of excessive fluid loss and also of increased sodium consumption. Individuals at the extremes of life may be at particular risk, and also those who have undergone certain medical procedures such as dialysis, and colonoscopy, or who have had intravenous fluid replacement or hyperalimentation [ 26 ].
Hypernatremia may be found at autopsy in wide range of a medical conditions and also following misadventure. Elevated sodium levels should therefore be suspected in cases where there is evidence of reduced fluid intake, and post-mortem levels should be measured.
Serum sodium has been shown to decrease after death at an average rate of 0. However, the decrease in sodium levels after death means that an elevated level is more likely to be of significance [ 26 ]. Although changes occur in post-mortem sodium levels these often remain stable for sufficient time to provide information that may be useful in determining the mechanism of death [ 26 ] For example, the ante-mortem serum sodium and chloride concentrations are reflected in post-mortem vitreous values, making it possible to diagnose hyponatremia or hypernatremia at the time of death [ 1613141625 - 28444951 - 59 ].
Madea and Lachenmeier [ 60 ] mentioned 17 cases of hypertonic dehydration showing increased vitreous sodium and urea values. There are also cases of increased vitreous sodium values not related to dehydration and therefore it has been concluded that prudence should be used in determining the cause of death on the basis of vitreous sodium and chloride values only [ 25 ].
The possibility of inflicted injury or feeding error should be suspected in infants who present with markedly elevated levels of sodium [ 26 ]. Glucose and ketones Diabetes mellitus is a chronic metabolic disease responsible for many deaths [ 61 ]. New onset of insulin-dependent diabetes mellitus often presents with Diabetic Ketoacidosis DKAwhich along with Hyperglycemic Hyperosmolar State HHSare the two main conditions causing death in the diabetic population [ 62 - 64 ].
The diagnosis of various metabolic conditions is often difficult to make post-mortem due to major changes in the blood and other tissues [ 65 ]. Elevated levels of glucose and ketones can be an indication of this condition and can be obtained and analyzed from VH post-mortem [ 63 ]. VH is the matrix of choice for this diagnosis because of post-mortem alterations involving glucose metabolic pathways, such as post-mortem blood glycolysis [ 66 ].
Three substances have been used to measure ketoacidosis: During ketoacidosis, BHB is found in the highest concentrations and seems to be the most specific post-mortem marker of ketoacidosis [ 5867 - 69 ].
The medical examiner is often faced with an elevated vitreous BHB that appears to have little or no bearing on the case [ 61 ]. The diagnosis of fatal metabolic complications in diabetes mellitus is difficult because of the lack of autopsy and histological findings. Moreover, these complications can occur in persons with no known diabetes [ 8 ].
Relationship between sudden natural death and abdominal fat evaluated on postmortem CT scans
A high VH glucose concentration in conjunction with a significant BHB concentration can be used to identify hyperglycemia and distinguish death due to DKA from ketoacidosis caused by other circumstances [ 64 ]. A high glucose concentration also indicates that an individual was a possible diabetic, a condition that may not have been diagnosed prior to death [ 64 ].
Of course, increased glucose concentrations may be seen in other causes of death, including post-mortem cases after prolonged agony, traumaemergency resuscitation attempts, or surgery [ 64 ]. Post-mortem diagnosis of hyperglycemia and ketosis can be achieved by biochemical analysis of VH [ 72 ]. An increase in the rate of glycolysis has been found in VH during the early post-mortem period, leading to a decrease in glucose concentrations [ 5146673 ].
Thus, low vitreous glucose concentration is not synonymous with hypoglycemia [ 73 ]. This drop in glucose concentration stops around 24 hours after death [ 5 ]. Most likely, in the early phase, the glucose in the vitreous will be consumed by surviving hyalocytes and inner retinal cells [ 54974 ].
After their death, an equilibration will gradually take place between the intra- and extracellular space [ 5 ]. The glucose is usually near zero within a short period [ 4974 ].
However, when blood glucose levels are abnormally high not all the vitreous glucose will be metabolized [ 514 ]. The concentration of glucose in vitreous is about half of the concentration in blood [ 75 ]. It has been proposed in previous studies that the BHB concentration in VH could be an alternative marker in the absence of an available blood sample [ 71 ].
However, further investigation is required to verify this suggestion and to determine a suitable reference range [ 64 ]. Therefore, glucose measurement is essential to determine hyperglycemia and, therefore, to distinguish between DKA and ketoacidosis from other causes. Some authors suggest VH glucose concentrations should be routinely measured where possible in all cases where BHB is detected in significant concentrations [ 64 ].
They also suggest that VH glucose concentrations should be routinely measured in all unexplained deaths, irrespective of whether a significant concentration of BHB is detected or not and especially in cases with risk factors for diabetes including obesity, old age or a history of mental health problems [ 64 ].
Many authors suggest that as glucose is broken down into lactate, one glucose molecule is converted into two lactate molecules, their combined concentrations should be used to determine hyperglycemia [ 516667277 - 79 ]. One report suggested a combined glucose and lactate values in vitreous or CSF over threshold values of However, a number of studies refute the idea of using glucose and lactate in combination. Multiple studies looked at cases to evaluate the diagnostic accuracy of the sum values of glucose and lactate in the VH or in CSF to estimate ante-mortem blood glucose levels and rule out fatal diabetic ketoacidosis as the cause of death [ 52582 ].
The studies concluded that ante-mortem hyperglycemia could be detected by measuring only glucose levels in the VH or CSF [ 52582 ]. Thus, the sum value of glucose and lactate in the VH or CSF did not add any further information when estimating antemortem blood glucose concentrations [ 52482 ].
Moreover, the use of the sum value could lead to an overestimation of cases of glucose disorders with fatal outcomes, such as diabetic ketoacidosis. Thus, the vitreous glucose concentration alone appears to be the most reliable marker to estimate ante-mortem blood glucose concentrations [ 52582 ]. They also concluded that the determination of acetoacetate levels does not add any further information in order to estimate the importance of ketonemia when glucose metabolic disorders are associated with ketoacidosis [ 82 ].
Glucose determination, together with the measurements of ketone bodies, urine glucose and glycated haemoglobin, can easily confirm the existence of a glucose metabolism disorder and a diabetic decompensation as a cause of death [ 25 ].
The supplementary determinations of glycated haemoglobin, acetone and other ketone bodies were also recommended in order to identify diabetic ketoacidosis [ 25 ]. However, a vitreous biochemical threshold for the diagnosis of significant ketosis is less clear. Threshold BHB levels of 2. Post-mortem vitreous BHB is a useful marker for DKA when levels are elevated and accompanied by an above threshold vitreous glucose level concentration [ 62 ].
Between Eye Differences Perhaps the most important concern in utilizing vitreous biochemistry emerges from the reported between-eye differences in the same pair of eyes at identical PMI [ 51 ].
For example, one study found significant differences in the same pair of eyes in regards to vitreous potassium concentrations [ 88 ].
It has been hypothesized that sample dilutions prior to analysis account for the between-eye differences in the same pair of eyes, and therefore measuring the samples undiluted has been suggested [ 88 ]. The results of a number of studies have since shown that there is no difference between eyes at the same PMI, including vitreous sodium, potassium, chloride, and sodium-potassium ratio [ 2051 ].
These findings are not unexpected as it is well known that autopsies of patients who die after a prolonged period of resuscitation and support in the ICU typically report multiple organ failure as the primary cause of death regardless of the different primary diagnoses [ 30 ].
A Pathophysiological Insight into Sepsis and Its Correlation with Postmortem Diagnosis
We ascribe our lower ICU autopsy rate to one of three possibilities. First, in our center, the physician caring for the patient during hospitalization may differ from the outpatient physician who has a long-standing rapport with the family. Additionally, when the patient is admitted to the ICU, the critical care team assumes primary care.
Thus, there may not be a single physician with a close enough relationship to the patient's next of kin at the time of death to obtain consent for an autopsy. Second, due to the frequent use of advanced high-tech investigative modalities available at our center, both physicians and family members may perceive that the autopsy will have a low yield. Third, when patients with advanced cancer die, physicians and family members often attribute the death to the expected complications of the malignancy.
In this circumstance, it is perceived that an autopsy is unnecessary.
Mediators of Inflammation
Our study has several limitations, including the retrospective study design and selection bias that may have occurred; physicians and family members of patients with premortem diagnostic uncertainty would have been more likely to pursue an autopsy than in cases in which all parties were certain of the diagnoses and the outcome was predictable.
Similar to prior studies [ 1315 ], we were unable to fully account for all the premortem diagnostic investigations that were performed on all the autopsied patients. Nevertheless, we believe that our findings may be extrapolated to similar critically ill cancer patients treated in general ICUs. The missed major diagnoses were commonly due to opportunistic infections and cardiac complications.
Our findings underscore the need for enhanced premorbid surveillance, monitoring, and treatment of infections and cardiopulmonary disorders in critically ill cancer patients.
However, given the limitations of present-day microbiologic evaluation and treatment and cardiac imaging at the ICU bedside, the autopsy remains an invaluable tool for retrospective diagnostic understanding of difficult cases, medical education, and quality assurance.
Competing interests The authors declare that they have no competing interests. All authors were involved in drafting the manuscript and have full access to the data and take full responsibility for its integrity. All authors read and approved the final manuscript. The role of autopsy in the intensive care unit. Clinical and autopsy diagnoses in the intensive care unit: Comparison of premortem clinical diagnoses in critically ill patients and subsequent autopsy findings.
Do autopsies of critically ill patients reveal important findings that were clinically undetected? Autopsy as quality assurance in the intensive care unit. Quality control in fatally injured patients: The relationship of pre mortem diagnoses and post mortem findings in a surgical intensive care unit. Does the length of stay in the intensive care unit influence the diagnostic accuracy? Eur J Emerg Med.