Clinical Case Study Assignment 2 - Nursing Process Worksheet

Name: Carly Hylton

Clinical Reasoning Cycle (CRC)

Consider the Patient Situation
Mr. Hennessey is a 66 yo male who was brought to the emergency room via ambulance. At 11am, his wife found him at home at the bottom of his basement
stairs on the ground mumbling and agitated. His wife called the ambulance, and, on the scene, the paramedics found him to be lying on the ground, shouting
and agitated and were unable to understand his speech as he was slurring and mumbling. Mr. H was unable to follow commands but was seen moving all 4
limbs spontaneously.

At 11:30am, vitals on scene were:

BP: 112/68; HR: 130 irregular; RR: 22; SpO2 96%; temp: 37◦C axillary
During transport via ambulance, Mr. H became ++ combative RASS +4 and was given Midazolam IM 1mg for which the response was that Mr. H was a
RASS +1 and that the transport could be completed to the ED.

His PMHx & medications

Active Smoker: 12.5 pack year
Active ETOH: active 2 bottles of wine/day
DM type 2: MetforminTM
HTN: EnalaprilTM [Ace inhibitor]
Atrial Fibrillation: PradaxaTM (dabigatran etexilate) [anticoagulant]
Statin: RosuvastatinTM
Osteoporosis: Os-calTM BID
Cirrhosis: Child-Pugh Class A
Previous hospitalization 1 year ago for alcohol overdose, was admitted for 5 days and returned home.

Social History as reported by wife on scene

Mr. and Mrs. H had a fight 5 days ago about his alcohol use and the police were called to the home when the neighbours heard yelling and the sound of
crashing. Mrs. H reported he had continued to drink alcohol since his prior hospitalization. She reported he had been neglecting himself, and his duties to
the home. She stated that he was becoming more forgetful and had been agitated and aggressive towards her. On the day of the fight, he had thrown plates at
her. When the police arrived, they were able to calm him down, he agreed to leave and sleep at a friend’s house that night. She refused to press charges.
Further, she reported the cost of his continued drinking and smoking was overwhelming as the cost of living was rising and they were on a limited income
since retirement. She reported she was considering leaving the home because of this. She stated after the fight, she told Mr. H he had to promise to quit
drinking “for good” if he wanted her to stay.

On arrival at the ED, Mr. H was not following commands. He was opening his eyes spontaneously however not looking at the staff or following gaze, he
continues to use inappropriate words and abnormal slurring speech, GCS: 11. He was seen spontaneously moving all limbs; however, he was not noted to be
moving his left foot. His left leg showed significant bruising and the left ankle was swollen ++. His peripheral pulses were present x 4 limbs. Mr. H was
breathing spontaneously with a soft abdomen. Given his continued agitation, he received midazolam 2mg and a CT head was completed, which came back
negative for any abnormal findings. A bedside x-ray revealed a fracture to the left lateral malleolus.
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Baseline vital signs in ED @ 13:00:

Labs in ED:
BP: 140/85
HgB: 141 g/L
RR: 21/min
HcT: 0.52
HR: 125/min irregular
A1c%: 9.1
02 Sat r/a: 99%
Random glucose: 7.7 mmol/L
Temp axillary: 37.3◦C
WBC: 25.1
Weight 99 Kg
Platelets: 140
Creatinine: 152
K+: 3.8 mmol/L
Mg2+: 1.32 mmol/L
Na+: 140 mmol/L
PO4: 1.04 mmol/L
CK: 4167 U/L
ALT: 56 U/L
Bilirubin Total: 7 mmol/L
Troponin: 141 ng/L

ABG: pH:7.27; HCO3: 20; CO2:57; Serum lactate: 9.0

Mr. H remained in RESUS. Thirty minutes later, he became so agitated and aggressive that a code white was called as he was grabbing the staff and
throwing punches at them. Midazolam 6mg and 2 mg Haldol IV was given and he continued to remain agitated and aggressive with staff. His vitals were
BP: 215/109; T: 37.3◦C axillary; HR: 136; RR:26; SpO2: 100% RASS +4. It was decided given the significant danger to the patient and staff as the patient
remained combative and severely agitated pulling at all his medical equipment and was not responsive to any verbal commands that Mr. H be intubated.
He underwent a rapid sequence intubation with propofol (150mg), midazolam (10mg), and succinylcholine (150mg). During intubation he became
hypotensive to 79/49 and hypoxic to 79% for 30 seconds. Neosynephrine 300mcg was administered, due to continued hypotension he was started on a
neosynephrine drip titrated to a MAP ≥65. He was placed on a ventilator on AC/VC; RR:15 PEEP 7, TV: 550 and placed on a propofol drip titrated to a
RASS 0/-1. A chest Xray confirmed placement of the ETT.

Mr. H was transferred to the ICU, where he was admitted under the primary admission diagnosis agitation not yet determined, rule out: delirium tremens,
hepatic encephalopathy, post ictal delirium. On admission to the ICU, an arterial line was placed to his left radial site, a triple lumen was placed to the right
jugular, a foley was inserted to monitor his ins and outs, and NGT was inserted, and admission order for bloods to be done included blood cultures, CHEM
10 and ABG including lactate TID; CBC, Coags, LFTs, CK DIE. A chest xray confirmed placement of NGT and the central line.
He was started on a loading dose of Keppra, Thiamine IV, Folic acid IV, multivitamin IV, CBGM QID with sliding scale Humulin R. He continued to
receive propofol titrated for a RASS 0/-1 and the neosynephrine was changed to a norepinephrine drip once the central line was confirmed titrated to a MAP
=>65.
He was also started on Ringer’s Lactate at 50 ml/h.

The next day an electroencephalogram (EEG) was done at bedside in the morning which came back negative, in the afternoon an MRI head was completed
which came back with mild chronic vascular atherosclerosis and mild bi-lateral frontal atrophy. His 6am bloods showed irregular findings for Mg2+: 0.50;
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PO4- : 0.70 and orders for PRN electrolyte replacements were inputted. The day shift nurse ensured appropriate electrolyte replacements occurred.

What are some of your conclusions? Which additional therapies could we consider? Where could this case progress to? What are some of the risks to the
patient given the therapies started? What psychosocial concerns might you have for this patient and family? Use the clinical reasoning cycle below to
answer the above questions, and the highlighted prompts to guide your responses.
Collect Cues/ Information
Review current information by reading the above case (e.g. handover reports, patient history, patient charts, results of investigations and nursing/medical assessments
previously undertaken)
Organize the most important information here (you can choose to do this by body system if that helps).
Neurological:
 On scene: agitation, incomprehensible speech (mumbling, slurred speech) with increased volume (shouting), possible fall (found on the bottom of his basement
stairs on the ground), unable to follow commands. Pt’s wife reports that pt was increasingly “forgetful, agitated, and aggressive” recently. Potential decrease in
alcohol consumption around 5 days prior (pt’s wife told pt to “quit drinking for good” to prevent her from leaving the home/relationship, pt drinks 2 bottles of
wine/day, previous hospitalization for alcohol overdose 1 year ago)
 During ambulance transport: pt was combative (RASS +4), received midazolam IM 1 mg, response was RASS of +1 post-administration of midazolam.
 ED (RESUS): GCS score of 11 (eyes opening spontaneously, not following commands but moving spontaneously, inappropriate words/incomprehensible speech
(slurred speech)). Not following gaze or directing gaze to staff. Received midazolam 2 mg IM for continued agitation. Remained agitated and became combative
30 minutes later; midazolam 6mg and 2 mg haldol IV, response was continued agitation and aggressive behavior (RASS +4) so pt was intubated. Underwent rapid
sequence intubation with propofol 150 mg, midazolam 10 mg, and succinylcholine 150 mg. Propofol drip titrated to a RASS 0/-1. CT head scan negative.
 ICU: DDx: delirium tremens, hepatic encephalopathy, post ictal delirium. Started on loading dose of Keppra, Thiamine IV. Propofol drip titrated to a RASS 0/-1
continued. EEG negative. MRI revealed mild chronic vascular atherosclerosis and mild bi-lateral frontal atrophy.
Cardiovascular:
 PMHx of HTN (Rx: enalapril) and Afib (Rx: pradaxa)
 On scene: BP: 112/68, HR: 130 irregular
 ED (RESUS): Peripheral pulses present x4 limbs. K+: 3.8 mmol/L, Troponin: 141 ng/L, CK: 4167 U/L. HR: 125/min irregular→136; BP: 140/85 (ED T1)→215/109 (ED
T2)→79/49 (intubation), neosynephrine 300 mcg administered, pt remained hypotensive so neosynephrine drip titrated to MAP ≥65 started.
 ICU: left radial arterial line, right jugular triple lumen placed (placement confirmed with chest xray). Order for CK and Coags DIE. Neosynephrine drip titrated to
MAP ≥65 continued via central line. Started on ringer’s lactate 50 ml/h.
Respiratory:
 On scene: RR: 22; SpO2 96%
 ED (RESUS): Breathing spontaneously upon admission. ABG: pH:7.27; HCO3: 20; CO2:57; Serum lactate: 9.0. Underwent rapid sequence intubation (with propofol
150 mg, midazolam 10 mg, and succinylcholine 150 mg). RR: 21/min→26, SpO2 99% RA (ED T1)→100% (ED T2)→79% (intubation). ETT placement confirmed by
xray. Ventilator on AC/VC; RR:15 PEEP 7, TV: 550.
 ICU: Order for ABG including lactate TID. Started on ringer’s lactate 50 ml/h.
Musculoskeletal:
 PMHx of osteoporosis: (Rx: os-cal)
 ED (RESUS): Pt not moving left foot, ecchymosis to left leg, left ankle edema, left lateral malleolus fracture revealed by bedside x-ray.
Gastrointestinal:
 PMHx cirrhosis (Child-Pugh Class A).
 ED (RESUS): Soft abdomen, pt weights 99 kg, ALT: 56 U/L, bilirubin total: 7 mmol/L

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 ICU: NG tube inserted; placement confirmed with chest xray. LFTs DIE.
Renal:
 ED (RESUS): Creatinine: 152
 ICU: Foley catheter inserted (in/out monitoring)
Endocrine & Metabolic:
 PMHx of DM type 2 (Rx: metformin). Rx rosuvastatin (PMHx of dyslipidemia?)
 ED (RESUS): A1C%: 9.1, random glucose: 7.7 mmol/L
 ICU: Order for CBGM QID, sliding scale Humulin R
Hematological & Immune:
 ED (RESUS): WBC: 25.1, platelets: 140, HgB: 141 g/L, HcT: 0.52
 ICU: Order for blood culture. CBC and Coags DIE.
Multi-system/other:
 On scene: T: 37◦C axillary
 ED (RESUS) Mg2+: 1.32 mmol/L, Na+: 140 mmol/L, PO4: 1.04 mmol/L, T: 37.3◦C axillary
 ICU: Folic acid IV, multivitamin IV administered. Mg2+: 0.50; PO4- : 0.70. Electrolyte replacement administered. CHEM 10 DIE
Functional assessment & Social Hx:
 Retired. Tobacco: 12.5 packs/year. Alcohol: 2 bottles of wine/day (previous hospitalization for alcohol overdose 1 year ago). Conflict between pt and wife 5 days
ago surrounding pt’s alcohol consumption, pt became violent (threw plates). Police called to scene by neighbors who heard “yelling and crashing” sound. Pt’s
wife refused to press charges. Pt’s wife reported pt “neglecting himself” and that pt’s role functioning at home has declined. Couple’s financial health affected by
pt’s tobacco and alcohol consumption as per pt’s wife. Pt’s wife told pt to “quit drinking for good” to prevent her from leaving the home/relationship.
Gather new information (e.g. undertake patient assessment)
What additional information would you like to know and why?
 What are the patient's current ABG and lactate levels? It's important to understand if the patient still exhibits mixed metabolic/respiratory acidosis and to
evaluate for hypoperfusion. Additionally, what is the patient's current oxygen saturation (SpO2)? This information is important for potentially adjusting
ventilator settings to enhance brain perfusion, especially considering the patient's neurological symptoms.
 An urgent electrocardiogram (ECG) should be obtained due to the patient's elevated Troponin levels (141 ng/L) and CK levels (4167 U/L), suggestive of MI (if not
already on continuous cardiac monitoring). Previous troponin and CK levels and any abnormal ECG findings (i.e. anything other than sinus rythym or Afib as he is
already known for Afib so this would be expected) should be reported to MD. Additionally, other causes for elevated troponin and CK should be explored if no
evidence of (N)STEMI is found (e.g. MI type II).
 Has the patient decreased alcohol consumption following the recent conflict with their wife 5 days ago? This information is crucial to assess the potential
contribution of delirium tremens to the patient's symptoms, findings, and behaviors as 3 delirium tremens usually occurs within 48-96 hours of withdrawal
(Hoffman & Weinhouse, 2024).
 Did the pt’s wife or anyone else observe signs of a seizure leading up to the pt’s hospitalization? This is important to assess post ictal delirium, in case someone
witnessed any signs of a seizure.
 Did the pt’s wife notice any sx of alcohol withdrawal in the 5 days leading up to pt’s hospitalization (nausea/vomiting, tremor, sweating, anxiety, reported
perceptual (tactile/auditory/visual) disturbances, headache, disorientation)? This is important to assess whether delirium tremens could explain some of the pt’s
sx, findings and behaviors.
 Did the patient's wife notice a gradual/insidious or sudden/acute onset of the patient's behavioral changes and symptoms? Understanding the timeline and
progression of symptoms would help to distinguish between conditions like hepatic encephalopathy, which typically has a gradual onset.
 I would like to review the MRI imaging findings to see what the pattern of frontal atrophy to see whether there is a “knife edge pattern” that is characteristic of
frontal dementia (Peet et al., 2021). Also, it would be interesting to read the radiology report to see if there are any areas of ischemia that could contribute to
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dementia (frontotemporal, vascular dementia etc) (Pluta, 2022).
 Current neurological assessment, including Glasgow Coma Scale (GCS), pupillary response, and other pertinent assessments, is necessary to monitor neurological
status and guide treatment decisions.
 We could recommend obtaining the pt’s ammonemia levels (ideally arterial ammonemia) as hyperammonemia would contribute to hepatic encephalopathy, and
we could recommend lactulose if has hyperammonemia (Mandiga et al., 2023). Assessment of bowel habits would be important, as constipation can increase
ammonia levels and exacerbate hepatic encephalopathy (Wolf, 2020). Lactulose could additionally help treat or prevent constipation.
 What are the results of the LFTs? INR? Does the pt have ascites? What is pt’s current child pugh score or class? This would help us understand pt’s liver
functioning.
 Does the pt show any signs of pain (tense or grimacing facial expression, protection or restless movements, muscle tension)? What is the pt’s CPOT score? This
would help us assess the pt’s pain given his left lateral malleolus fracture.
 Given that the pt’s creatinine level was elevated upon admission, which would indicate an alteration in renal functioning, I would like to know the pt’s in and
outs. Is there decreased urine output? We could also recommend obtaining the pt’s BUN levels to further assess renal functioning.
 Given the pt’s elevated WBC count, I would like to know the results of the blood culture, his current temperature, and I would like to assess for any other
signs/sx of infection.
 What supports does the pt’s wife/family need at this time? This could help create a collaborative partnership with the pt/family to optimize pt care.

Clinical Reasoning Cycle (CRC)

Process Information
Discriminate: distinguish relevant from irrelevant information; recognise inconsistencies; narrow down the information to what is most important; recognise gaps
What information do you feel is the most relevant to the current situation?

High priority information Low priority information

 Behavioural changes (agitation, incomprehensible speech, forgetful,  PMHx of HTN (Rx: enalapril) and Afib (Rx: pradaxa), irregular HR
agitated, and aggressive/combative)  Started on ringer’s lactate 50 ml/h.
 Potential decrease in alcohol consumption around 5 days prior (pt’s wife  A1C%: 9.1, random glucose: 7.7 mmol/L
told pt to “quit drinking for good”, pt drinks 2 bottles of wine/day)  ICU: Folic acid IV, multivitamin IV administered. Mg2+: 0.50; PO4- : 0.70.
 GCS 11 upon admission (while values are abnormal, electrolyte replacement has been
 MRI revealed mild chronic vascular atherosclerosis and mild bi-lateral administered so it is not high priority at this time but important to keep in
frontal atrophy. mind for monitoring).
 Troponin: 141 ng/L, CK: 4167 U/L  Retired.
 ABG: pH:7.27; HCO3: 20; CO2:57; Serum lactate: 9.0.  Tobacco: 12.5 packs/year.
 SpO2 99% RA (ED T1)→100% (ED T2)→79% (intubation)  Couple’s financial health affected.
 BP: 140/85 (ED T1)→215/109 (ED T2)→79/49 (intubation), prescribed
neosynephrine
 ALT: 56 U/L, bilirubin total: 7 mmol/L
 Creatinine: 152
 WBC: 25.1

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Interpret: analyse data to come to an understanding of signs or symptoms; compare normal vs abnormal.
What information do you feel is normal and abnormal (and why)?

Normal Abnormal (and why?)

 CT head scan negative, EEG negative.  Conflict with spouse, pt’s wife reported pt “neglecting himself” and that
 On scene: BP: 112/68 (Rx: enalapril) pt’s role functioning at home has declined, couple’s financial health
 Peripheral pulses present x4 limbs. affected. Pt drinks 2 bottles of wine/day, previous hospitalization for
 K+: 3.8 mmol/L alcohol overdose 1 year ago. These all correlate with DSM V criteria for
 On scene: RR: 22; SpO2 96% alcohol use disorder (APA, 2013).
 ED (RESUS): Breathing spontaneously upon admission, RR initially 21, SpO2  Behavioural changes (agitation, incomprehensible speech, forgetful,
99% RA (ED T1)→100% agitated, and aggressive/combative). RASS +4. GCS 11. These are
 Platelets: 140, HgB: 141 g/L, HcT: 0.52 abnormal behavioral changes that are evidence of altered mental status
 T: 37◦C axillary→37.3◦C that could correlate with delirium tremens, hepatic encephalopathy, post
 Mg2+: 1.32 mmol/L, Na+: 140 mmol/L, PO4: 1.04 mmol/L ictal delirium.
 MRI revealed mild chronic vascular atherosclerosis and mild bi-lateral
frontal atrophy: These are abnormal findings that are not typically
associated with hepatic encephalopathy but are more suggestive of
dementia (Peet et al., 2021; Sabayan et al., 2023).
 HR: 130 irregular→125/min irregular→136: Tachycardia and irregular HR
correlate with the PMHx of Afib, these findings are all abnormal.
 Troponin: 141 ng/L, CK: 4167 U/L: These findings are indicative of cardiac
involvement and possible MI.
 BP: 140/85 (ED T1)→215/109 (ED T2)→79/49 (intubation), neosynephrine
administered: ED T2 BP (215/109) is hypertensive crisis. Subsequent
hypotension could have been provoked by intubation. Neosynephrine
administered to increase BP.
 ABG: pH:7.27; HCO3: 20; CO2:57; Serum lactate: 9.0: Indicate mixed
respiratory and metabolic acidosis and hypoperfusion of organs
 ED RR increased to 26: could be a compensatory response to respiratory
acidosis.
 SpO2 79% (intubation): Hypoxemia. While this could be explained by the
intubation procedure, it would be important to know what the post-
intubation SpO2 is.
 PMHx of osteoporosis: (Rx: os-cal), pt not moving left foot, ecchymosis to
left leg, left ankle edema, left lateral malleolus fracture revealed by
bedside x-ray. These are all abnormal findings; pt’s osteopororis puts him
at higher risk for fractures.
 PMHx cirrhosis (Child-Pugh Class A), ALT: 56 U/L, bilirubin total: 7 mmol/L:
Indicates liver dysfunction and potentially correlates with DDx of hepatic
encephalitis.
 Creatinine: 152: Indicates impaired renal function.
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 PMHx of DM type 2 (Rx: metformin). Rx rosuvastatin (PMHx of
dyslipidemia?), A1C%: 9.1, random glucose: 7.7 mmol/L: abnormal
findings, DM type 2 not under control.
 WBC: 25.1: Suggestive of infection or inflammatory response
 Mg2+: 0.50; PO4- : 0.70. Electrolyte replacement administered: electrolyte
imbalance, potentially due to renal dysfunction or other metabolic
disturbances.
Relate: discover new relationships or patterns; cluster cues together to identify relationships between them
Note and cluster the pieces of information you believe relate to one another (and how)
Alcohol use→ cirrhosis → hepatic encephalopathy → behaviour changes:
 Conflict with spouse, pt’s wife reported pt “neglecting himself” and that pt’s role functioning at home has declined, couple’s financial health affected. Pt drinks 2
bottles of wine/day, previous hospitalization for alcohol overdose 1 year ago. These all correlate with DSM V criteria for alcohol use disorder (APA, 2013).
 Alcohol consumption (2 bottles of wine/day) and potential alcohol use disorder could have contributed to the development and potential worsening of cirrhosis.
 Worsening cirrhosis could have led to hepatic encephalopathy, especially because pt was not taking any prophylactic treatments before hospitalization
(lactulose, thiamine)
 Hepatic encephalopathy could explain behavioural changes (agitation, incomprehensible speech, forgetful, agitated, and aggressive/combative, RASS +4)
Alcohol use→ conflict with spouse → alcohol withdrawal → delirium tremens → behaviour changes:
 Pt’s spouse reports a conflict 5 days ago surrounding alcohol use, in which she made the pt promise to “quit drinking for good”. If pt indeed did significantly
decrease or stop his alcohol consumption, this could have led to delirium tremens which usually occurs 2-5 days after alcohol consumption is ceased (Hoffman &
Weinhouse, 2024).
 Hepatic encephalopathy could explain behavioural changes (agitation, incomprehensible speech, forgetful, agitated, and aggressive/combative, RASS +4)
Rx rosuvastatin (PMHx of dyslipidemia?) + PMHx of HTN (Rx: enalapril) → Mild chronic vascular atherosclerosis and mild bi-lateral frontal atrophy:
 Dyslipidemia could lead to accumulation of plaque in blood vessels in the brain causing atherosclerosis and hypertension can further damage the vessel walls
contributing to atherosclerosis which could in turn contribute to frontal atrophy (Sabayan et al., 2023).
Osteoporis → left lateral malleolus fracture → WBC: 25.1:
 Pt’s osteopororis puts him at higher risk for fractures.
 The fracture, pain and the inflammatory response could explain his elevated WBC (TBC by blood culture).
ABG: pH:7.27; HCO3: 20; CO2:57; Serum lactate: 9.0 → RR↑26
 ABG and lactate results indicate respiratory and metabolic acidosis and hypoperfusion of organs.
 RR increase to 26 could be a compensatory response to respiratory acidosis.
PMHx cirrhosis (Child-Pugh Class A) + ALT: 56 U/L + bilirubin total: 7 mmol/L + creatinine: 152 → potential hepatorenal syndrome
 Advanced cirrhosis increases the risk for renal dysfunction (hepatorenal syndrome) (Ranasinghe et al., 2023).
Infer: make deductions or form opinions that follow logically by interpreting subjective and objective cues; consider alternatives and consequences
Where do you think this situation will progress to, based on your data?
 Liver transplant may need to be considered if pt’s cirrhosis has advanced to child-pugh class B or greater (Tsoris & Marlar, 2023).
 While some data point to a potential acute cause for the pt’s sx (e.g. potential delirium tremens as evidenced by possible alcohol cessation 5 days ago), MRI
finding of mild chronic vascular atherosclerosis and mild bi-lateral frontal atrophy are not characteristic of delirium tremens or hepatic encephalopathy and
suggest ongoing neurodegenerative processes (Peet et al., 2021; Sabayan et al., 2023). Therefore, the pt may have many complex factors contributing to the
observed behavioural changes that require further investigation and management.
 Elevated troponin (141 ng/L) and CK (4167 U/L) levels are critical and indicative of cardiac involvement and possible MI. This could possibly be a complication of
other disease processes (e.g. MI type II).
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 MI could lead to decreased perfusion of the brain, exacerbating the patient's altered mental status. Given the patient's neurological symptoms and MRI findings,
prompt and comprehensive management of both cardiac dysfunction and neurological dysfunction is essential to prevent further deterioration and mitigate the
risk of additional neurological sequelae.
Identify Problems/Issues
Synthesize facts and inferences to make
a definitive statement of the person’s,
family’s or community’s
issues/problems/concerns
What are your top nursing care
priorities, in order? Enumerate them
for clarity, and provide a short
rationale).
1. Impaired gas exchange
Rationale: Pt had respiratory acidosis as -The patient will demonstrate clear
per ABGs upon admission, had
increased respiratory rate (possible
compensation mechanism), last
reported SpO2 was 79% upon
intubation
2. Acid-based imbalance
Rationale: Pt had mixed
respiratory/metabolic acidosis as per
ABGs on admission.
3. Impaired cardiac tissue perfusion
Rationale: Elevated troponins and CK.
4. Risk of impaired organ and
peripheral tissue perfusion
Rationale: Elevated lactate, and
impaired cardiac tissue perfusion could
lead to impaired organ and peripheral
tissue perfusion.
5. Risk of alcohol withdrawal and
delirium tremens
Rationale:
Pt’s wife made him promise to “quit
drinking” 5 days ago which would
correlate to the onset of delirium
tremens, which could explain
behavioural changes
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Establish Goals Take Action Evaluate Outcomes
Describe what you want to happen, a Select a course of action between Evaluate the effectiveness of actions and
desired outcome, a time frame different alternatives available outcomes. Ask: “has the situation
What are your related goals of care? What are the evidence-informed improved now?”
nursing intervention(s) related to the How would you assess the
problem? (These can include medical effectiveness of the intervention, and
interventions.) Include a rationale. what would improvement look like?
In less than 24 hours: -Auscultate & suction secretions PRN  Normal arterial blood gas (ABG)
-Elevate head of bed to 30-45 degrees readings and reduced dependence
airway maintenance, as indicated by the -Obtain ECG stat (Byrne et al., 2023) on mechanical ventilation.
absence of abnormal breath sounds -Retest troponin levels 1 hour after  Stable renal function and
post-suctioning. obtaining initial troponin levels, if maintenance of fluid equilibrium.
-The patient's ABG levels, respiratory troponin levels remain elevated, retest  Normalized lactate levels, showing
rate, and oxygen saturation will be 3 hours after obtaining initial troponin enhanced tissue perfusion.
within normal range. levels (Byrne et al., 2023)  Improved mentation and increased
-Improved cardiac tissue perfusion will -Patient should be on continual responsiveness.
be observed through a reduction in monitoring of vital signs, pulse  The patient and their family exhibit
troponin and CK levels. oximetry, fluid and electrolyte status, strengths, adaptations, and coping
-Adequate perfusion will be evident by and neurological functioning (Hoffman mechanisms, resulting in
stable vital signs, MAP ≥ 65, normal & Weinhouse, 2024) heightened resilience.
blood lactate levels, and detectable -Thiamine and glucose should be
peripheral pulses. administered as per MD order to
-The patient's cognitive function will prevent Wernicke’s encephalopathy
improve and remain within normal (Hoffman & Weinhouse, 2024)
parameters. -Assess pain using CPOT
-Normal input and output will be -Monitor neurovascular signs
maintained by the patient.
-Goals of care will be collaboratively
discussed, determined, and
documented with the pt/family.
-The pt/family will demonstrate
enhanced understanding of alcohol use
disorder, alcohol withdrawal, and will
exhibit improved coping strategies and
resilience
 Reflect on Process
Reflect what you have learnt from this process and what you could have done differently. Reflect on how this was guided by or how you can integrate Strengths-Based
Nursing and Healthcare into this process. Consider how interprofessional communication and teamwork would support this process. Reflect on the potential impact of
stigmatization surrounding alcohol-related conditions on this process. Share your thoughts based on these leading statements.

I have learned about the many ways that one disorder (possible AUD) can give rise to numerous pathologies, potentially manifesting simultaneously. Reflecting on this
experience, I would adopt a different approach to the CRC process in the future. Instead of presuming a singular underlying pathology, I would try to consider the
possibility of various contributing processes to mitigate bias bias when trying to interpret the information. Likewise, interprofessional communication and teamwork was
important to support this process as this case required a multifaceted approach. From a SBN lens, it was very evident that the person integral SBN value was of utmost
importance in this case (Gottlieb, 2014). The patient was shaped by his environment and relationship (Gottlieb, 2014). Also, it was extremely important to create a
collaborative partnership with the spouse to understand the case and optimize care for the patient (Gottlieb, 2014). This case also allowed me to reflect on the potential
impact of stigmatization surround alcohol-related conditions. I found myself questioning why the patient hadn't received adequate treatment for AUD following their last
hospitalization or continued prophylaxis like thiamine. This made me reflect on my own experience as a nurse, and I have noticed that patients with AUD are often quick
to be dismissed, especially if they do not show readiness to change. This deficit-based approach not only overlooks opportunities for preventive healthcare but also
exacerbates future health complications, ultimately resulting in higher costs to the healthcare system. As a nurse, it prompts me to advocate for more holistic and
proactive approaches to care, ensuring that individuals with AUD receive the support and interventions they need for better long-term outcomes.

Reflect on New Learning

Consider a similar situation in your clinical practice where a patient/client presented with altered level of consciousness and/or communication disorders. Reflect on what
you’ve learned from this case that applies to your practice, and how you would care for this patient/client differently following this exercise. Share your thoughts based
on these leading statements.

I have cared with patients with alcohol withdrawal syndrome, sometimes exhibiting altered levels of consciousness and impaired speech. I have learned from this case
that it is important to take a proactive approach to gathering data rather than passively waiting for the patient to regain communicative abilities. This is important for
optimizing treatment efficacy and mitigating the risk of severe complications such as delirium tremens. One valuable lesson learned from this case is the importance of
gathering information as early as possible. Instead of solely relying on the patient's ability to communicate their alcohol consumption history, it’s important to seek
collateral information from family members, friends, or caregivers, if available. By doing so, the nurse can gain crucial insights into the patient's alcohol consumption
patterns and anticipate potential life-threatening complications such as delirium tremens. By taking a proactive approach appropriate interventions tailored to the
patient's specific needs can be initiated earlier. Early identification of risk factors for severe withdrawal symptoms enables healthcare providers to implement preventive
measures and provide timely pharmacological interventions, ultimately enhancing patient outcomes and minimizing the likelihood of adverse events.

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