This is the group of deaths in which alcohol related arrhythmias will be present. In this study, five of our seven highlighted arrhythmic deaths were in Davies category 5. There have been numerous speculations as to the cause and mechanism of death. Severe metabolic disturbances including high levels of free alcoholic ketoacidosis smell fatty acids do probably play a major role due to the effect on the Krebs Cycle. Heavy alcohol use can also impair the liver’s ability to synthesize and release glucose. These two factors decrease the body’s normal levels of readily available energy, and it responds by breaking down fat and producing ketones.
This is why diagnosis and subsequent treatment can sometimes be challenging, but it’s crucial to receive a proper and timely diagnosis to obtain the correct treatment. Because alcoholic ketoacidosis (aka) kills approximately 7% of patients who use alcohol daily, it is a serious complication. Ketoacidosis is caused by a lack of glucose in the blood, and insulin levels in the pancreas are low to zero. Alcohol can cause stomach irritation and vomiting, even after a person is unconscious. Dehydration and excessive ketone production can cause a person to develop diabetic ketoacidosis (DKA), which can lead to death.
Alcoholic ketoacidosis: review of current practice and association of treatments to improvement
Interestingly, despite this, ischaemic heart disease in this study was still the single commonest cause of death in the alcohol excess group accounting for 16.7% of deaths. It may be that some of these 10 cases were indeed SUDAM cases, but at the present time, the criteria for SUDAM need to remain strictly defined until such time as it is more fully understood, allowing the boundaries to be widened. It is also likely in the authors’ opinion that in patients with preexisting cardiac disease (hypertrophic or ischaemic) that alcohol acts synergistically to potentiate fatal arrhythmia in some cases. There is just simply not enough data on this at this time from this study to answer this conclusively.
In the two cases in which there was toxicology available, alcohol was present at non-fatal or low levels, as shown in previous studies [6,8]. These seven cases represented 0.5% of deaths undergoing coroner’s post mortem. In 2005, 230,000 deaths were referred to Coroners in England and Wales, accounting for 45% of all deaths .
Vitreous humor endogenous compounds analysis for post-mortem forensic investigation
There may be concomitant features of dehydration or early acute alcohol withdrawal. Bedside testing reveals a low or absent breath alcohol, normal blood sugar, metabolic acidosis, and the presence of urinary ketones, although these may sometimes be low or absent. An altered level of consciousness should prompt consideration of alternative diagnoses such as hypoglycaemia, seizures, sepsis, thiamine deficiency, or head injury. Arterial blood gas and biochemistry studies reveal a raised anion gap metabolic acidosis without evidence of lactic or diabetic ketoacidosis. Growth hormone, epinephrine, cortisol, and glucagon are all increased.
- Ketoacidosis is caused by a lack of glucose in the blood, and insulin levels in the pancreas are low to zero.
- There are inevitable limitations of a post-mortem study performed under current patterns of practice in the UK.
- Fever was seen in only two patients, both with other likely underlying causes.
- Examination should reveal a clear level of consciousness, generalised abdominal tenderness (without peritoneal signs), and tachypnoea.