My Rotation Objectives and progress to meeting them.
1. Understand the physiological mechanisms of shock states, understand the difference between the three main types of shock, and know how to treat a patient experiencing shock and what parameters to monitor.
Almost everyone patient that I saw was undergoing some form shock, therefore I had lots of practice in meeting this objective. One resourse that I found very useful for learning about shock states was: http://www.ccmtutorials.com/.
Hypovolemic (Decreased PCWP, increased SVR (body is compensating), decreased CO, and decreased BP. Treat with fluid replacement and vasopressors/inotropes (dopamine/dobutamine)
Cardiogenic (Increase PCWP (heart isn't pumping very well, so increase wedge pressure), decreased CO, decreased CO) Treat with dobutamine 1st line,
Septic/Distributive (decreased SVR (lots of vasodilations), decrease BP, decrease CO
Treat with fluids, and norephinephrine (1st line) or dobuatmine (consider if CO is low)
Role of Steriods: controversial
Monitoring: HR, BP, MAP, CVP, if swan catheter- (PCWP, and CI)
2. Improve my understanding of Vasopressors and Inotropes. Understand the difference between the different agents, and when to use one agent over another
Dopamine: acts on Dopamine, B2, B1, A2, A1: inotropic, chonotropic, and VC effects
-consider in hypovolemic shock
Dobutamine: has more vasodilatory properties as well as inotropic and chontropic effects
--> first line cardiogenic shock
Epinephrine: used in ACLS: inotropy, chonotropy and VC
Norepinephrine: lots of A1 -Vasocontriction (as well as A2 and B1)
--> first line in sepsis , can also be used for profound hypotension in hypovolemic and cardiogenic shock SE: ischemia (bowel, extremeties, heart)
3. Apply Acid-Base principles to my patients
I was able practice my acid-base skills on all my patients. Please see the clinical experiences box for more info on this.
4. Learn about some of the pharmacokinetic, pharmacodynamic changes that effect the critically ill patients.
I am now aware that there are differences in PK and PD in the critically ill. See clinical experiences box for more details. For example in all of my patients who were on vancomycin, I used a VD of 1L/kg instead of a VD of .7L/KG.
I feel that I have better understanding of pharmakinetics after this rotation. Sean encouraged be to use Pharmokinetic equations to recommend appropiate doses and predict what sort of response an individual patient would get from their doses. I also had an oppurtunity to practice phenytoin pharmacokinetics.
Prior to this rotation I had little experience dealing with lab reported MICs and at first I wasn't sure what do with them. I now understand how I can apply them to my patients therapy-using knowledge of the basic PK principles.
--> Dose =Css x Cl x Tau Cl= Vd x K Cpeak=Dose/Vd
5. Learn about conditions that commonly effect the critically ill Ex VAP, CRBSI, delirium and be able to recommend appropiate therapies
I encountered this conditions often on our daily found and had theraupeutic discussions about them with sean
On past rotations one of my personal goals is always to feel like a functioning clinical pharmacist in the particular clinical area by the end of the four weeks. Unfortunately I don't feel that I was able to accomplish that goal with this rotation- I found the critical care environment very different that other areas that I have worked- and still need further skills, knoweledge and experience to feel competent and comfortable. That being said, I was told by Sean at the beginning of the rotation that my goal shouldn't be to become "him" by the end of the rotations, instead it should be to try to learn as much possible. I feel like I did learn a lot on this rotation,. I had the oppurtunity to really apply all of that undergrad human physiology, pharmacology and pharmacokinetics to my patients and use that knowledge to understand what was happening in their bodies and what I could do as a pharmacist to help normalize things. Also, I feel that I was able to really refine my head- to toe approach on this rotation.
Presentations, Docs I've Created, Important Articles Encountered on this Rotation
The NICE-Sugar Trial
This is the journal article that I spoke about during my journal club presentation. It was large MC trial and one of the principal investigators was by attending physician on my team during the rotation.
Journal Club Handout
This is my prentation handout for the journal club.
This a presentation of delirium that we gave to BCIT student nurses.
Geets et el
This is a study that compared LDUH vs enoxaparin for critically ill trauma patients. It found that LMWH had an ARR of 8-9% compared to UH
Critical Care Medcine Tutorials
This a resource that I found very useful especially for respiratory failure (and learning about ventilators) shock and sepsis.
Topics Discussed : All topics discussed with Sean unless otherwise notes
HIT and the 4 T's (Thrombocytopenia, Timing, Thrombosis, and Other Causes
Hemodynamic Monitoring Parameters
Mechanical Ventilation and Intrepating Respiratory Lab Values
Feeding (Discussed with Dietician
Stress Ulcer Prophylaxis
Bilirubin and Drug Causes of elevations
Catheter Related Bloodstream infections
DVT prophylaxis in the critically ill
Conditions in whcih troponin may be elevated without over ichemic heart diesase
The Safe Study: A comparison of Albumum and Saline for Fluid Resuscitation in the ICU
--> albumum was as safe as saline
PK/PD in the critically Ill
DRESS: Drug rxn with eosinophilia and systemic symptoms (drugs involved include phenytoin
Spinal Shock vs Neurogenic Shock
Role of Gabapentin and baclofen in spinal cord injury neurogenic pain/spasticity
PROWESS: Efficacy and Safety of Recombinant human activated Protein C for severe sepsis: NNT 16 but NNH may be higher than in study--> bleed risks
CORTICUS: Hydrocortisone Therapy for Patients with Septic Shock
Clinical Experiences and their Learning Points:
1. BK 64 YO Male with complete C5 Block after an bicycle accident. This patient presened post-op in neurogenic shock. He later developed a VAP.
Learning points/ Questions I was asked:
Neurogenic Shock vs Spinal Shock: Spinal shock is the clinical syndrome characterized by the loss of neurological function and autonomic tone below the level of the spinal cord lesions. It usually persists<24 hours, but can last for several days. Spinal shock on the other hand is a result of hypotension from the loss of descending sympa pathways in the spinal cord. It often includes bradycardia (especially in younger patients) Management includes fluid management and vasopressors (and inotropes if bradycardic)
LMWH of UF for DVT prop in Acute Spinal Cord Injury: Pts with an acute SCI have the highest incidence of DVT among all hospitalized groups. The Chest guidlelines Grade 1c: recommend against using LFUH, instead recommend using LMWH or the combination of IPC and LDUF and LMWH. Useful studies: DETECT, and Geerts et al ( enox vs LDUF in critically ill pts, found an ARR for 9with enox bid). In other critically ill patients, it is still appropiate to use LDUF SC.
Role of Gabapentin in Spinal Cord Related Neuropathic pain: Gabapentin has been found to be beneficial in spinal cord related neuropathic pain- not a lot of large good quality studies though.
Role of Baclofen in Spinal injury spasticity: There is insufficient evidence to recommend baclofen or any other agents for spinal injury spasticity
2.AC:64 M with acute resp failure post open heart surgery (AVR, aortic root reconstruction) after having staph epi of his atrial valve. ICU adm: cardiogenic and septic shock, VAP, hyperbilirubinemia, several episodes of pulseless Vtack, CCRT, leukocytosis
How dose CRRT affect pharmaokinetics? CRRT: Continuous renal replacement therapy. Drug Cl= sieving coefficient (specific for different drugs) x Qd (dialysis flow rate) Qr (replacement rate) Quf (ultrafiltration)
What is TRALI (transfusion related acute lung injury) and is there any indication for steriods? Traili- acute lung injury during 1st 6 h post transfusion. Causative agents: antikeukocyte antibody, biologically active substances. No good on data on use of steroids- only anecdotal data. This patients respiratory failure seemed to fit TRALI.
ID: This patient provided a lot of learning opportunities for ID- specifically endocarditis, vanco, unexplained prolonged leukcystosis ( WBC remained >20 well on many broad spectrum abx, and having no positive blood cultures. Pseudomonas VAP.
This patient also had hyperbilirubinemia and elevated LFTS. CT and ultrasounds revealed no causes, we tried to eliminate as many drugs as possible that could effect his liver- ranitidine--> PPI, nozinan was also d/c. This pt rec'd several days of amiodarone therapy and many boluses for his pulseless VT- when I drew a timeline of event it seems like the amiodarone could have been contributing to the elevated LF, however I wouldn't expect it to effect bilirubin unless serious hepatic injury did occur,
3.DC 77 M with 2 and 3rd degree burns on low extremities when pt was burning his fluids. Escharotomy in ER--> pts Fi02 req increased, rhabdo CK>14000 positive urine myoglobin, UGIB, severe grade D esophagitis
PK changes in burn patients and critically ill patients
Increased VD: increased fluid extravasations, fluid loss (BURNS early phase), compartmental fluid accumulations (ascites etc)
Increase Cl: Burns late phase, acute leukocytosis, hyperdynamic sepsis phase
Decreased Cl: decrease renal fx, older age
Rhabdo and renal failure secondary to burns: Rhabdomyolysis can arise secondary to direct thermal effect, compartmental syndrome or following an electrical injury. The release myglobin or uncong Hg into the systemic circulation results in blockage of renal tubules, constrictions of afferent arterioles and generation of oxygen free radicals--injures renal tubular cells--renal failure
4. LC-80 y.o Male with pseudomembranous colititis secondary to C diff. Rec'd a hemicolectomy- surgeons goals was to avoid total colectromy. Recent past admission for sepsis: polymicrobial secondary to liver abscess. Past adm complicated by common femoral DVT and C diff
Intracolonic Vancomycin administration/ Treatment of pseudomembranous colitis secondary to C diff.
The gold standard for pseudo membranous colititis is total colectomy, however in this patient the surgeon hoped that parts of the colon could be saved. When we met the patient he was post op hemicolectomy but still had an open abdomen, and an discontinuous GI tract (middle parts staples shuts) He was receiving IV metronidazole however the surgeon also wanted to give him vancomycin. I did a lit search with sean, we found several case reports case report and recommended a method of intracolonic administration with a vanco concentration and had been used before and did not result in further toxicity to the colon. We recommended a vanco solution with a [ ] of 1g/L. In the case reports it was admistered via a colonic tube in 250 boluses q6h. However in this patient, the surgeon was able to surgically insert a line into his abdomen and provided a continuous irrigation/infustion at 40 mg/hr. Pt had a rectal tube that colect the soln as it drained through the colon. We ordered a vanco level a few days into therapy as one study found that significan systemic absorption was possible in intracolonic admin- our vanco level was 0.9. This met our goal of minimal systemic absorption with hopefully maximally local effect.
5.The Dr. HOUSE case:
TWC 83 Y/O M HPA: Pt collapsed while sitting at home at table (?seizure) Presented with Decrease LOC, weakness, bradycardia, hyotension, and visual hallucinations (in week leading up to incident)
This patient was a mystery- when my rotation ended we still did not what caused his admission, however he did develop VAP and a NSTEMI during his ICU stay.
Full ID workup:All cultures were negative (blood, resp, urine CSF,cryptococcal, herpes etc)
organophoshate poisoning was queryed as the pt had a picture that partially resembled a cholinergic toxidrome (moisis, increased secretions and bradycardia) and no other identifiable cause. I did full a med history, and found no possible source of the poisoning. C
Cholinesterase levels were ordered and although they were slightly low, they were did not support a poisoning diagnosis.
phenytoin: This patient was started on phenytoin due to his seizure on admission. I practiced my phenytoin PK stills and did calculations to predict how to decrease dose and when to give next dose when pts level was supratherapeutic.
Acid-Base disturbances: pH 7.45, PCo2- 50. Po2- 94, HCo3- 34)
1. ID emia: Akalemia
2. Primary Process: Metabolic Alkosis,
3. AG?No AG
4: Incompete compenstation 1:0.6-- therefore resp acidosis is also occuring.
Pt was given acetazolamide for 1 day. Labs the following morning: (7.39,52,87, 30)
PC02 increased and didn't decrease therefore metabolic alkalosis isn't the primary prosess- resp acidosis is still occuring. Acetazolamide was then discontinued
This case really helped me understand the pharmacists role in acid-base balance.