Blood alcohol content (bac) depends on each of the following except:

Overview of methods

BAC measurements can be obtained from living or deceased subjects, from a variety of body fluid or tissue specimens (Caplan, 1996). The standard is direct blood alcohol measurement because it best represents the effects of alcohol on the brain and can be obtained from a living person. In addition to body fluids (blood, urine, saliva, sweat), BAC can also be derived from breath samples and it can also be estimated under controlled conditions.

One source of confusion in the literature is the methods of expressing BAC. BACs can be expressed in two formats: (a) weight by volume (w/v) or (b) weight by weight (w/w). In the more common w/v format, BAC is calculated using grams or milligrams of alcohol in a given volume of blood (usually 100 ml or its equivalent, 1 dl). Thus, BAC in grams per deciliter is equivalent to grams per 100 ml, and can be expressed as grams percent (0.10%) or milligrams percent (100 mg%). See Table 2 for two BACs expressed in common units found in the research literature.

Table 2. BAC expressed in common units found in the research literature

W/vW/wBreath analysis0.10%0.10 g/100 ml0.10 g/dl100 mg/dl1 g/l0.095%0.10 g/210 l breath0.08%0.08 g/100 ml0.08 g/dl80 mg/dl0.8 g/l0.076%0.08 g/210 l breath

Note: W/w = w/v ÷ 1.055 (i.e., specific gravity of blood).

In the following sections we will present an overview of common methodologies associated with blood, breath, urine, saliva, and transdermal analysis. We also discuss methods of retrospective reconstruction using formulas for deriving BACs. For each method, we will present the primary advantages and disadvantages of the approach.

Accident and Emergency Departments.

Blood alcohol concentrations have been measured in patients attending accident and casualty departments with head and other injuries; some 50% were found to have raised values, usually in the region of 100–300 mg/dL (22–65 mmol/L). Similarly, 40% of patients attending an accident and emergency service during the evening hours had positive breath-alcohol readings, one-third of these corresponding to a blood alcohol greater than 80 mg/dL (17 mmol/L).49

Alcohol measurements in accident and emergency departments may grossly underestimate the frequency of chronic alcohol abuse. In patients attending such a department, randomly screened by questionnaire for problem drinking, measurement of breath alcohol showed a diagnostic sensitivity of only 22%.50 Almost 80% of positive breath tests were thought to represent casual drinking only.

Up to one-third of drivers involved in road traffic accidents and with blood alcohol concentrations exceeding 80 mg/dL (11 mmol/L) have been found to show additional biochemical changes suggestive of chronic alcohol abuse.

Abstract

Although blood alcohol concentrations are most commonly used to assess the degree of alcohol intoxication, blood is not always available for analysis, and it may be in poor condition, especially in postmortem investigations. Therefore, analysis of alcohol in other body fluids is common in forensic laboratories. The alcohol concentration in a body tissue or fluid is generally proportional to the water content of that tissue or fluid. For example, if the water content of a body tissue is 10% higher than that of blood, the tissue’s alcohol content should be 10% higher than that of blood. This is the basis for estimating blood alcohol concentrations from alcohol concentrations in other body fluids and tissues. Knowledge of the alcohol content of oral fluid, sweat, and tears can be used to make reliable estimates of coexisting blood alcohol concentrations. However, such estimates are more complicated when dealing with body fluids existing in isolated compartments where there is slow or very little exchange of alcohol between blood and the isolated fluid, for example, bile, eye fluid, and urine. Nevertheless, in postmortem investigations, knowledge of the alcohol content of any one of these and other fluids can often be used to estimate the minimum blood alcohol concentration existing some time before death.

2.2 Acute Intoxication

As blood alcohol levels increase in humans, the impact of alcohol on cognitive abilities, psychomotor performance, and vital physiologic functions increases (Naranjo and Bremner, 1993, Table 2).

Table 2. Clinical Manifestations of Blood Alcohol Concentration

Blood Alcohol Level mg%Clinical Manifestations20–99Loss of muscular coordination
Changes in mood, personality, and behavior100–99Neurologic impairment with prolonged reaction time, ataxia, incoordination, and mental impairment200–299Very obvious intoxication, except in those with marked tolerance nausea, vomiting, marl-zed ataxia300–399Hypothermia, severe dysarthria, amnesia, Stage 1 anesthesia400–799Onset of alcoholic coma, with precise level depending on degree of tolerance
Progressive obtundation, decreases in respiration, blood pressure and body temperature
Urinary incontinence or retention, reflexes markedly decreased or absent600–800Often fatal because of loss of airway protective reflexes from airway obstruction by flaccid tongue, from pulmonary aspiration of gastric contents, or from respiratory arrest from profound central nervous system obstruction

Source: Reproduced with permission (Mayo-Smith, 2009)

With chronic use, tolerance to the effects of alcohol develops, so the functional impact of a specific amount of alcohol is dependent on a number of factors including degree of tolerance, rate of intake, body weight, percentage of fat and gender.

Alcohol intoxication initially impacts the frontal lobe region of the brain, causing disinhibition, impaired judgment, and cognitive and problem-solving difficulties. At blood alcohol concentrations between 20 mg% and 99 mg%, along with increasing mood and behavioral changes, the effects of alcohol on the cerebellum can cause motor-coordination problems. With blood alcohol levels of 100–199 mg%, there is neurologic impairment with prolonged reaction time, ataxia, and incoordination. Blood alcohol levels of 200–399 mg% are associated with nausea, vomiting, marked ataxia and hypothermia. Between 400 mg% and 799 mg% blood alcohol level, the onset of alcohol coma can occur. Serum levels of alcohol between 600 mg% and 800 mg% are often fatal. Progressive obtundation develops with decreases in blood pressure, respiration, and body temperature. Death may be caused by the loss of protective airway reflexes, aspiration of gastric contents or respiratory/cardiac arrest through depressant effects of alcohol on the medulla oblongata and the pons (Table 2, and Mayo-Smith, 2009).

Severely intoxicated individuals may require admission to the hospital for management in specialized units with close monitoring and respiratory support. In individuals with coma, alternative causes must always be investigated, such as head injury, other drug use, hypoglycemia, or meningitis.

Aspiration of Gastric Contents

Blood alcohol levels greater than 250 mg/dl produces profound effects on the respiratory centre in the brain causing respiratory paralysis, and also on the glottic reflex, increasing the likelihood of aspiration of gastric contents. Many deaths that occur from acute alcohol poisoning are associated with aspiration of gastric content, subsequent asphyxia and death.

Classically, the aspiration of gastric content causes an acute chemical pneumonitis. This is characterized by acute inflammation of the major airways and the lungs in response to direct contact with the noxious material. Aspiration of acidic contents, such as gastric content, is associated with immediate injury to the trachea, bronchi and alveoli. On direct vision at bronchoscopy, diffuse bronchial erythema is seen. The degree of injury is directly related to the pH of the gastric content, with low pH materials having the most profound effects. The resultant process is that of acute lung injury, with release of proinflammatory cytokines and inflammatory cell infiltration. The acute inflammatory process plays an important role in the sequelae of aspiration pneumonia. Sequelae primarily involve hypoxaemia that can be life-threatening (Johnson and Hirsch, 2003). There are many factors that play a role in the formation of hypoxaemia and are shown in Table 4.

Table 4. Factors contributing to hypoxaemia in aspiration pneumonitis

Re.ex bronchospasm

Decreased surfactant activity

Atelectasis

Subsequent ventilation–perfusion mismatch

Intrapulmonary shunting

Direct alveolar damage

Note: Sequence of events as a result from aspiration of gastric contents after acute alcoholic intoxication.

In people who have suffered acute alcohol poisoning, the primary event that will lead to their death will be hypoxaemia.

3 Diagnosis of Fatty Liver Disease

3.1 Elevated Liver Enzymes

Serum ADH, serum transaminases aspartate transaminase [AST] and ALT are major indicators of alcohol-induced injury. Author established hepatocyte and Kupffer cell enzymes participating in liver injury and drug metabolism at different points in cell as shown in Figure 41.2. In fatty liver, diffused liver injury was shown associated with elevated liver tissue metabolite contents, serum metabolites and nuclear magnetic resonance (NMR) relaxation data with visible changes in liver magnetic resonance imaging (MRI) scan (see Figure 41.4; Table 41.1).

Figure 41.4. Focal hepatic steatosis is shown by different imaging modalities including US (a), CT (b), in phase MRI (c), out phase MRI (d), T2wt MRI (e), T2FS MRI (f), T1Grad MRI (g), and out of phase susceptibility MRI (h).

Source: http://radiopaedia.org/articles/focal_fat_infiltration.

Table 41.1. Comparative NMR Biochemical Correlation Analysis of Liver with Diffused Injury by Different Methods Using NMR Relaxation Times, In Vitro NMR Spectroscopy, In Vivo MR Spectroscopy, Tissue Metabolites, and Serum Enzyme Levels

MethodNormal liverDiffused liver injuryIn vitro pulsed NMR
 T1 ms
 T2 ms
448 ± 20 ms
88 ± 7 ms
939 ± 11 ms
144 ± 9 msIn vitro NMR spectroscopy
 Phosphocreatine/creatine
 Phosphorylcholine
 Taurine
0.48 mM
7.2 mM
5.75 mM
1.06 mM
61.3 mM
23 mMIn vivo NMR spectroscopy
 Glutamine
 Aspartate
36.1 mM
6.27 mM
35.2 mM
2.7 mMBiochemical tissue metabolites
 Phospholipids
 Triglycerides
113.8 ± 3.9 mg%
89.7 ± 4.8 mg%
168.9 ± 5.6 mg%
139.9 ± 3.6 mg%Biochemical serum levelsa
 Serum glutamate pyruvate transaminase
 Alkaline phosphatase
 Bilirubin
18.5 ± 1.9 IU
39.5 ± 7.8 IU
1.5 ± 0.2 mg%
140.9 ± 15.4 IU
239.9 ± 23.4 IU
4.2 ± 0.6 mg%

aIU is defined as μ moles substrate used per minute per mg enzyme protein.

Source: Sharma, R., 1995. PhD (MRI) dissertation thesis submitted at Indian Institute of Technology, New Delhi.

Effects of Food on Blood Ethanol Concentration

The peak BEC is reduced when alcohol is consumed with or after food. Food delays gastric emptying into the duodenum. This attenuates the sharp early rise in BEC seen when alcohol is taken on an empty stomach. Food also increases elimination of ethanol from the blood. The area under the BEC/time curve (AUC) is reduced (Figure 4). The contributions of various nutrients to these effects have been studied, but small, often conflicting, differences have been found. It appears that the caloric value of the meal is more important than the precise balance of nutrients.

In animal studies ethanol is often administered with other nutrients in liquid diets. The AUC is less when alcohol is given in a liquid diet than with the same dose of ethanol in water. The different blood ethanol profile in these models may affect the expression of pathology.

However, food increases splanchnic blood flow, which maintains the ethanol diffusion gradient in the small intestine. Food-induced impairment of gastric emptying may be partially offset by faster absorption of ethanol in the duodenum.

What 4 factors is BAC determined by?

What is BAC and what 4 factors affect BAC?

What does blood alcohol level depend on?

What 3 things affect a person's blood alcohol content BAC )?