Derek is admitted to the emergency department critically unwell. Consider the presenting symptoms as outlined in the social history, video clips and medical records and address the following; a) Provide and interpretation of Derek’s ABGs.

Derek’s blood gases are as follows
PaO2 80mm/Hg
PaCO2 52mm/Hg
PH 7.25
HCO3 30 The results show that Derek has respiratory acidosis. According to Porth and Matfin, (2009) respiratory acidosis is a condition was an acid imbalance occurs in the body. During gas exchange, the exchange of gas is impaired and results in excess carbon dioxide (CO2) being absorbed into the blood stream, initiating the formation of an acid, making the blood more acidic (Porth & Matfin, 2009). The PH drops as there is little ventilation of the alveolar, and compensation results in the production of hydro carbon dioxide (HCO2) (Farrell & Dempsey 2005). Respiratory acidosis may be caused by injury to the respiratory centres, diseases of the lungs, blockage of the airway and respiratory disorders (Porth & Matfin, 2009).

b.) Provide two possible reasons for the ABG’s based on Derek’s history and presentation.

The cause for Respiratory acidosis in Derek could have been caused by a respiratory disorder such as COPD which he has been diagnosed with since 1997, and was asked to cease smoking but up to date he has continued to smoke 20-30 cigarettes per day. Porth and Matfin, (2009) explain that conditions of the respiratory system may cause impairment of gas exchange. Respiratory acidosis could also have been caused by poor diet intake. Derek has hypercholesterolemia and type 2 diabetes mellitus, he lives close to convenience stores and often consumes take away foods. The proximity of these stores and the distance from the nearest train station probably encourages him to take fast food. These foods are high in carbohydrates and they will produce CO2 within the body.

c.) Provide the pathophysiology for the two reasons identified.

COPD
Chronic Obstructive Pulmonary Disease is often characterised by ongoing and recurrent obstruction of the airways (Budweiser, Jorres & Pfeifer, 2008). According to the Australia Institute of Health and Welfare, (2011) smoking is the leading cause of COPD. In COPD fibrosis and inflammation occurs to the bronchial wall and the mucosal glands become enlarged causing excessive secretions, which causes impaired airflow to the lungs (Farrell & Dempsey, 2011). COPD is the presentation of emphysema, were there is enlargement of airspaces and destruction of lung tissue and chronic bronchitis were there is obstruction of the small airway caused by chronic secretions. (Budweiser, Jorres & Pfeifer, 2011).
In emphysema there is loss of elasticity of the lung tissue, which is caused by proteases; these are enzymes responsible for the digestion of protein (Budweiser, Jorres & Pfeifer, 2011). According to Porth and Matfin, (2009) Irritants such as cigarette smoke cause inflammatory cells to shift into the lung triggering the release of proteases a usually anti protease is not adequate to neutralise the amounts of protease especially on smokers. The loss of elasticity in the lungs causes the increase in airspaces and results in hyperinflation and increase in total lung capacity Porth & Matfin, 2009), this means that the next breath of air is taken before exhalation is complete.
Bronchitis is the inflammation of the bronchi, which are air passages that connect the trachea to the lung tissues (Budweiser, Jorres & Pfeifer, 2011). When the bronchi become inflamed there is excess production of mucous secretions in the lining of the bronchi (Porth & Matfin, 2009). Viruses normally cause inflammation but irritants such as dust, inhaled chemicals such as cigarette smoke may also cause it (AIHW, 2011). When bronchitis becomes chronic, there is damage to the small airway and breathing will eventually become difficult (Budweiser, Jorres & Pfeifer, 2011). . Chronic health behaviours such as smoking are usually the cause of chronic bronchitis (AIHW, 2011).

Increased carbon dioxide production
The body produces CO2 during metabolism. Metabolism is a chemical process involving the breakdown of nutrients into building blocks. According to Porth and Matfin, (2009) a diet high in carbohydrates produces more CO2 during metabolism, as it requires extensive metabolism.
The lungs and liver are responsible for the elimination of CO2 during gas exchange (Budweiser, Jorres & Pfeifer, 2011). In the case study Derek has a diet intake that is high in carbohydrates and consumes more than the recommended standard drinks of alcohol which also produce CO2 during metabolism (Farrell & Dempsey, 2011). The increase in CO2 intake and its poor elimination because of compromised airway integrity may have contributed to the perfusion of CO2 into the blood stream making it acidic (Budweiser, Jorres & Pfeifer, 2011).
Because CO2 can cross the blood brain barrier it may cause vasodilation; widening of the blood vessels by relaxation of the smooth muscle causing headaches and psychological deficits (Budweiser, Jorres & Pfeifer, 2011).

Question 2 (20 marks)
It is likely that Derek will require assistance with his breathing.
a) Discuss which type of ventilation would be the most appropriate for Derek and outline the correct nursing management.

Noninvasive positive pressure ventilation (NPPV), NPPV is used for COPD patient with pH less than 7.35 and PaCo2 greater than 45mm/Hg (Caples, 2005).

Derek is having a moderate to severe exacerbation of chronic obstructive pulmonary disease (COPD) due to daily heavy cigarettes consumption. On the arrival to emergency department, he was suffering Dyspnoea, rapid shallow breathing, his pH was 7.25 and PaCO2 52mm/Hg.
Performing NPPV on Derek may improve oxygenation and promote ventilation during exacerbations because the positive pressure stents airways open and reduces inspiratory muscle effort. It improves respiratory acidosis, increase pH, eases breathlessness on Derek (Gavaghan, 2006).

Nursing management for NPPV:
Once NPPV is commenced, monitor priorities include response to noninvasive treatment, respiratory and hemodynamic stability, tolerance of ventilation, detection of noninvasive failure, and identification of air leaks around the interface. Physiological measures gas exchange parameters, ventilator parameters, and work of breathing (pH, PaCo2, respiratory rate, accessory muscle use, chest wall motion), level of consciousness, and hemodynamic status (heart rate, blood pressure, capillary refill). Also monitor cough and secretions frequently. Inability to effectively mobilize secretions may warrant adding humidification to the NPPV system, along with administration of mucus thinning agents, expectorants, or both (Rose, 2012)(Caples, 2005).

Compliance is directly to comfort. If eye irritation occurs, causes by airflow escaping or humidification, use eyedrops or ophthalmic lubricant as ordered. If patient develops ear pain and nasal and sinus congestion, provide goof oral care, saline spray, or decongestants and reassess air flow and mask fit (Rose, 2012).

Change body position at least every 2 hours to decrease chances of atelectasis and pneumonia as part of overall care with HOB elevated at least 30 degrees or higher unless contraindicated (Rose, 2012).
Pain and anxiety can be optimally managed with reassurance, teaching and medications. Medications should be used with caution, and reassess the patient for sedation. Frequently assess mental status, vital signs, work of breathing, and ability to protect the airway to help prevent fatigue or intolerance. Stay alert for hemodynamic instability (Rose, 2012) (Gavaghan, 2006).

b) Identify any precautions that you would take based on Derek’s clinical history and presentation.

In the case study, Derek is a chronic alcohol abuse patient with Delirium Tremens who is suffering COPD due to living condition and heavy smoking, he has had a recent trauma to occipital area of skull, MRI suggestive of Korsakof’s Dementia and confusion noted.

The history and Mental Status Examination (MSE) are the most important diagnostic tools which have to be obtained to make an accurate diagnosis and intervention, as well as Glasgow Coma Scale (GCS). A GCS measure the level of consciousness, especially Derek has had a head injury, experienced hyperventilate and became unconscious during the arrival to emergency department. It is determined by three factors: amount of eye opening, verbal responsiveness, and motor responsiveness (SIGN, 2009). A MSE has to be done in order to evaluate and perform any procedure effectively. This is to assess Derek’s level of cognitive ability, appearance, emotional mood, speech and thought patterns at time of evaluation (Folstein, 1975).

Korsakoff’s Dementia affects patient learning new information and the main symptom is unable to remember recent events. Derek is likely to lose the memory of committing to hospital and with a medical history of depression, he is most likely to experience anxiety and panic once he is conscious. Successful application of noninvasive ventilation requires patient cooperation and stable mental status, nurses need to help Derek to remain calm before applying intervention (Alzheimer’s Australia, 2012).

Derek is suffering from COPD, prescribed nebulised Anticholinergics and Bronchodilators can be delivered concurrently with noninvasive ventilation or during breaks from ventilator support. Anticholinergic helps enlarge the airways, making breathing easier and also reduce the amount of mucus produced by the airways (Lori, 2010). Ipratropium and salbutamol are commonly used in COPD patients.

Derek is also suffering alcohol withdrawal symptoms Delirium Tremens which causes agitation, hallucinations and confusion on him (Gavaghan, 2006). Nurses and staff need be aware of the sign and symptoms, assess his alertness and consciousness frequently. Medication Benzodiazepines maybe recommended for detoxification and reduce symptoms if necessary (Gavaghan, 2006).

Nutrition intake is specifically important for Derek as he lives with poor diet life style, and COPD patient may find it difficult to eat with breathless (Elliott, 2004). This is further compromised if they are unable to remove the mask for sufficient time to masticate food. Liquid supplements are an alternative but nasogastric feeding may be more appropriate, particularly acutely and oral medication can be given easily. Proper nutrition can help reduce carbon dioxide levels and improve breathing together with the use of noninvasive positive pressure ventilation (Elliott, 2004). Also support Derek on reducing tobacco use during intervention, nicotine patches apply when necessary.

Question 3 (2.5 marks)
Review Derek’s social history and use information gained from the videos to estimate the amount of alcohol Derek is currently consuming per day in standard drinks per day.

Based on social history information and videos, he drinks several cans of lager and cider every night and gets through 2-3 bottles of vodka each week. In the video Derek said that he drank a tumbler of whisky in the morning before he goes to work. The formula for calculating standard drinks is suggested by Australian Government Department of Health: Volume of Container in Litres multiplied by the percentage of alcohol volume multiplied by 0.789 equals the number of standard drinks. 0.789 is the specific gravity of ethyl alcohol. It’s hard to calculate his alcohol consuming because we do not know the volume of his drinking. According to the Australian Government Department of Health “A standard drink is any drink containing 10 grams of alcohol. One standard drink always contains the same amount of alcohol regardless of container size or alcohol type.” Just estimated that if Derek drinks 3 cans of beer every night and 1 can beer is 375ml equal to 0.8 units, his daily beer consuming is 0.8x3=2.4 units. A unit of vodka is approximately 25ml. If the bottle is 750ml, then 750 divided by 25 is 30 units and Derek drink 2-3 bottles is 60-90 units per week, 8.6-12.9 units per day. Derek’s daily alcohol consumes is about 11-15 standard drinks.

Question 4 (15 marks)
Derek history indicates that he currently meets the DSMIV diagnosis for alcohol abuse. a) Briefly outline the biological effects of alcohol on the brain

Alcohol affects brain chemistry by altering levels of neurotransmitters (Yeung, Ralph & Nieuwenhuis, 2007). Alcohol increases the effects of the inhibitory neurotransmitter GABA in the brain and result in a decreased sensitivity of GABA-A receptors to both alcohol and GABA itself (Yeung et al, 2007). Alcohol appears to actually change the genetic makeup of the neuron and thus change the structure of the receptor proteins generated by the cell (Yeung et al, 2007). Because of the damage to the function of the GABA inhibitory system, the CNS tends toward hyper excitability, resulting in the anxiety, tremors, disorientation, and hallucinations associated with alcohol withdrawal (Yeung et al, 2007). Chronic exposure to alcohol may also increase the sensitivity of glutamate receptors, and since glutamate is an excitatory neurotransmitter this would contribute further to CNS hyper excitability (Yeung et al, 2007).

In Cerebral cortex, alcohol depresses the behavioral inhibitory centers, making the person less inhibited; it slows down the processing of information from the eyes, ears, mouth and other senses; and it inhibits the thought processes, making it difficult to think clearly (Moselhy et al, 2001). In Cerebellum, Alcohol affects this center of movement and balance, resulting in the staggering, off-balance swagger (Moselhy et al, 2001). In Hypothalamus and pituitary, alcohol depresses nerve centers in the hypothalamus that control sexual arousal and performance (Moselhy et al, 2001). Although sexual urge may increase, sexual performance decreases (Moselhy et al, 2001). By acting on the medulla, alcohol induces sleepiness. It can also slow breathing and lower body temperature, which can be life threatening (Moselhy et al, 2001).

b) Why seizures may occur in alcohol withdrawal and why diazepam is useful for treating alcohol withdrawal?

Symptoms typical of withdrawal include agitation, seizures, and delirium tremens and it occur primarily in the central nervous system (Kovacs, 2003). Withdrawal seizures occur within 48 hours of alcohol cessations and occur either as a single generalized tonic-clonic seizure or as a brief episode of multiple seizures (Kovacs, 2003). Repeated periods of acute intoxication followed by acute detoxification have profound effects on the brain and are associated with an increased risk of seizures as well as cognitive deficits (Kovacs, 2003). Researchers have shown that the flow of calcium ions into brain cells via voltage-gated calcium channels plays an important role in the generation of alcohol withdrawal seizures, because blocking this flow suppresses these seizures (Prosper, 2009). Using a careful analysis of correlations between the course of alcohol withdrawal seizures and the expression of calcium currents, researchers found that the enhancement of total calcium current density in pre-clinical animal studies occur prior to the onset of alcohol withdrawal seizures (Prosper, 2009). "These preliminary findings are the first to indicate that altered calcium channel activity contributes to the occurrence of alcohol withdrawal seizures," explains by Prosper N'Gouemo (2009).

Diazepam is used to help reduce these withdrawal symptoms (Stehman & Mycyk, 2013). Diazepam is a benzodiazepine (Stehman & Mycyk, 2013). It controls the withdrawal symptoms until the body is free of alcohol and has settled down (Stehman & Mycyk, 2013). Benzodiazepines are used to treat the psychomotor agitation most patients experience during withdrawal and to prevent progression from minor withdrawal symptoms to major ones (Stehman & Mycyk, 2013). In general, long-acting benzodiazepines with active metabolites are preferred because they seem to result in a smoother course with less chance of recurrent withdrawal or seizures (Stehman & Mycyk, 2013). Benzodiazepines exert their effect via stimulation of gamma-aminobutyric acid (GABA) receptors, causing a decrease in neuronal activity and relative sedation (Stehman & Mycyk, 2013).

c) Describe the role of Vitamin B1 (Thiamine) in the brain and why vitamin B1 is commonly prescribed in alcohol misuse.

Thiamine, also known as vitamin B1, is an essential nutrient required by all tissues, including the brain (Smith & Randall, 2012). Thiamine is a helper molecule required by three enzymes involved in two pathways of carbohydrate metabolism (Smith & Randall, 2012). Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells to building blocks of proteins and DNA as well as brain chemicals, a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke–Korsakoff syndrome, which is found predominantly in alcoholics (Smith & Randall, 2012). The human body itself cannot produce thiamine but must ingest it with the diet (Smith & Randall, 2012). Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells (Smith & Randall, 2012).

Thiamine deficiency is common in people who are alcohol-dependent due to their poor diet, nutritional status, the presence of gastritis which can affect its absorption and also the fact that it is a coenzyme in alcohol metabolism (Sgouros & Baines, 2004). Alcoholics are often deficient in various nutrients which can cause severe complications during alcohol withdrawal (Sgouros & Baines, 2004). The vitamins of most importance in alcohol withdrawal are thiamine and folic acid (Sgouros & Baines, 2004). The vitamins of most importance in alcohol withdrawal are thiamine and folic acid (Sgouros & Baines, 2004).

Reference

Alzheimer’s Australia. (2012). Alcohol related dementia and Wernicke- korsakoff syndrome. Retrieved from https://www.fightdementia.org.au/common/files/NAT/2012_NAT_HS_AD_18_AlcoholRelatedDementia.pdf
Australian Institute of Health and Welfare, (2011). Asthma is Australia 2011 with a Focus on chronic obstructive pulmonary disease. Retrieved from http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=60129544677
Australian Government Department of Health. (2012). Standard drinks guide. Retrieved from: www.alcohol.gov.au
Budweiser, S., Jorres, R.A., & Pfeifer, M. (2008). Treatment of respiratory failure in COPD. International Journal of COPD, 3 (4), 605-618. Retrieved from http://www.ncbi.hm.nih.gov
Caples, S., Gay, P. (2005). Noninvasive positive pressure ventilation in the intensive care unit: a concise review. Crit Care Med. 2005:33, 2651-2658.
Elliott, M, W. (2004). Non-invasive ventilation for acute respiratory disease. British Medical Bulletin 2004. 72, 83-97. Retrieved from http://bmb.oxfordjournals.org/content/72/1/83.full.pdf+html
Farrell, M., & Dempsey, J. (2011). Smeltzer and Bare’s textbook of medical-surgical nursing. (2nd Ed). Broadway: NSW, Lippincott Williams & Wilkins
Folstein, M, F., Folstein, S, E., McHugh, P, R. (1975). Mini Mental State. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975:12(3),p189–198.
Gavaghan, S., Jeffries, M. (2006). Your patient’s receiving noninvasive positive pressure ventilation. Nursing. 2006:36, p46-47.
Kovacs, G. L. (2003). Natriuretic peptides in alcohol withdrawal: Central and peripheral mechanisms. Current Medicinal Chemistry, 10(23), 2559-2620. doi:http://dx.doi.org/10.2174/0929867033456459
Lori, D, C., Judith, M, J. (2006). Enhanced delivery of nebulized salbutamol during non-invasive ventilation. Journal of Pharmacy and Pharmacology. 2006:58(11), p1553-1557.
Moselhy, H. F., Georgiou, G., & Kahn, A. (2001). Frontal lobe changes in alcoholism. Alcohol & Alcoholisa. 36(5): 357-368.
Porth, C.M., & Matfin, G. (2009). Pathophysiology: concepts of altered health states. (8th Ed). Philadephia: PA, Lippincott Williams & Wilkins
Prosper, N. G. (2009). New Understanding of Why Seizures Occur With Alcohol Withdrawal. Georgetown University Medical Center.
Rose, L. (2012). Management of critically ill patients receiving noninvasive and invasive mechanical ventilation in the emergency department. Open Access Emergency Medicine. 2012:4, p5-15.
Sgouros, X., & Baines, M. (2004). Evaluation of a clinical screening instrument to identify states of thiamine deficiency in in patients with severe alcohol dependence syndrome. Alcohol Alcohol 39(3): 227–232.
SIGN. (2009). Early management of adult patients with a head injury Quick reference guide. Retrieved from http://www.sign.ac.uk/pdf/qrg110adult.pdf
Smith, J. P., & Randall, C. L. (2012). Anxiety and alcohol use disorders: Comorbidity and treatment considerations. Alcohol Research, 34(4), 414-431. Retrieved from http://search.proquest.com/docview/1430978706?accountid=10382
Stehman, C. R., & Mycyk, M. B. (2013). A rational approach to the treatment of alcohol withdrawal in the ED. The American Journal of Emergency Medicine, 31(4), 734-754. doi:http://dx.doi.org/10.1016/j.ajem.2012.12.029
Yeung, N., Ralph, J., & Nieuwenhuis, S. (2007). Drink alcohol and dim the lights: The impact of cognitive deficits on medial frontal cortex function. Cognitive, Affective and Behavioral Neuroscience (Pre-2011), 7(4), 347-355.