Nursing Interventions

This care study aims to outline the care provided to a patient during one 12hour shift. It will present the patients cause and course of ICU admission, identify problems both potential and actual, focussing particularly and two main problems. The nursing interventions preformed will be critically analysed and supported with research. Finally the care will be critically evaluated areas of possible improvement will be outlined.

Patient chosen is a 36yr old male pseudonym ‘Frank’ chosen for the purpose of confidentiality. Frank was day one post re- do orthotic liver transplantation (OLT) with roux -en-y anastomosis. He had his initial OLT for Primary sclerosing cholangitis secondary to auto-immune hepatitis preformed 5 days previously and
required and urgent re-do transplant due to Hepatic vein thrombosis not responsive to conservative treatment. Prior to his re-do transplant he had required CRRT due to acute kidney injury(AKI) related to large blood loss of 2.5litre due to coagulopathy related to liver failure. He was currently receiving CRRT.
Frank has a past medical history of auto immune hepatitis, Ulcerative colitis (total colectomy with ileostomy formation in 08 with recurrent adhesions, stomal varices, osteoporosis, Left bundle branch block (Asymptomatic).
He is a single man with both his elderly parents NOK.He was unable to work due to long term illness and lives with his parents 10miles away from the hospital.

Autoimmune hepatitis is a chronic hepatitis characterised by auto immune features, generally including the presence of circulating autoantibodies and a high serum globulin concentration (Krawitt 2006). This results in the body initialling in error an immune response to the liver cells and causing inflammation damage and death of the liver cells. Primary sclerosing cholangitis is the inflammation, scarring and death of the bile ducts.Ulcerative colitis is one of the risk factors

Hepatic artery thrombosis occurs in estimated 2.5% of liver transplants with aprox 50% requiring retransplantation(Stange et al 2003). It was in franks case diagnosed following routine ultrasound of liver ducts and Doppler to assess blood flow from the hepatic arteries.
ARF in liver disease is common and can occur due to renal hypo perfusion or increased renal vascular resistance. (Betrosian et al 2007) and occurs in aproximatley 23% of chronic liver failure patients (Agarwal et al 2009)

ASSESMENT
Frank has a GCS of 9/15. He had previously been on sedation and analgesia. But was currently having a sedation vacation as recommended by kress et al (2000). He was eye opening to pain and obeying commands. Richmond agitation score(RASS) was -2 light sedation.
On respiratory assessment Frank was intubated and ventilated on Pressure support ventilation (PSV)requiring minimal support of PS 8 PEEP 5 fio2 .24. ABG supported adequate ventilation and oxygenation. Respiratory rate 16 regularly work of breathing was normal and relaxed. Lung fields clear on auscultation. Productive cough on suctioning aseptically using size 12 (Pederson et al) Cuff inflated at 30cmh2 (Stewart et al) with Achieving adequate tidal volumes of 6mls per Kg as recommended by ARDs net 2000.

. Frank was maintaining a mean arterial pressure of 68mmg on 28 mc/hr. of Noradrenaline which was administered through a dedicate lumen of a central line and labelled accordingly. The MAP of 65mgh was identified patient parameter as recommended by le Doux as cited in Delinger et al 2009 to ensure adequate perfusion of the vital organs including renal perfusion. Alarms were set within patients parameters. Pulmonary artery flotation catheter was in situ with systolic 21mmgh, diastolic 9mmgh MAP 13 svo2 76% and estimated cardiac output 8.8 wedge pressure of 6 mmgh as performed by intensives. Central venous pressure of 3mmgh. Lines were transduced a phlebosatic axis, pressure 300mmgh. PAFC secured at pillow sutures secure syringe deflated and locked measured as 60cm as checked with previous shift. Large bore rapid infuser remained in situ since surgey.
On examination Frank had widespread peripheral oedema upper and lower extremities. Hypothermic. Left bundle branch block on ECG. HB 8.0 pale peripherally to feet pulses present on Doppler related to alpha effect of Noradrenaline. Terlipressin QDS, 2.5 litres

renal no urine output post op had been on CRRT since the intra operative period. Exchange 30mls/kg/hr. heparin due to thrombosis

Frank had a wide bore NGT on free drainage. He was not receiving enteral feeding as post biliary reconstruction and roux loop anastomosis of the biliary tree , Enteral feeding is not recommended in the first 48hrs post operatively to reduce the risk of biliary leakage at the anastomosis.(Welsh et al 2004) Stoma at ileostomy site was pink , protruding and functioning small amount of fluid. Abdomen was slightly distended firm to touch with transplant surgery site dressing dry and intact. Two Wallace drains were insitu with large amount of haemoserous output from the right drain. Bowel sounds were present

DEFICENT FLUID VOLUME RELATEED TO SURGERY.
Hypovolemic refers to the decrease in volume of circulating blood caused by either actual loss of volume extra cellular space or the inappropriate distribution of fluid in the intravascular space i.e. third spacing ( Al-khafaji and Webb 2004)
In franks case on assessment he was displaying signs of hypvolemia. He was on inotropic support to maintain a map above 65mmgh. His Cvp was 2, with his PAFC wedge pressure of 8. On examination he had widespread peripheral oedema indicating third spacing.Periperal odema was asseseds by pushinf on bony prominence for 5 seconds . Odema is classified as mild-severe or +1-=4 (Kirton 1996)14 His oral mucosa was dry. His lactate was raised at 3 indicating lactic acidosis.

Treatment of the problem was multifactorial and involves continuous communication with the multi-disciplinary team, Monitoring patient for response to treatment, and observing and treating side effects of condition and treatments.
The use of CVP as an indicator of fluid status is debated. CVP is dependent on venous return to the heart, right ventricular compliance, peripheral venous tone and posture (Al Khalil and Webb 2004) some or all of these may be present in the vulnerable ICU population and as a result leave space for unreliability. There is little concrete evidence to support the use of CVP monitoring (Ahrens 2010) and current developments such as technologies to accurately measure stoke volume may be future everyday practice
Franks jugular venous pressure was measured to estimate intravascular fluid volume. Not present. Moist mucous membranes, good skin turgor, and prompt capillary refill.

Considering frank had received four units of RCC intra operatively and his haemoglobin was 8 as recommended by Hebert et al 1999) fluids were prescribed by the physician. 500mls of colloid fluid was prescribed. A continuous debate between the choices of fluid for fluid resuscitation exists . Colloid fluids contain large molecules than crystalloids and are argued that these large molecules poorly diffuse outside the vascular space thereby reducing the leakage of fluid to the extra vascular space and maintaining cardiac output for longer thereby reducing volume required for favourable result. (Moranville et al 2010) However in a Meta-analysis of research of evidence of effect of crystalloid versus colloid fluids, there was no clear benefit of either on mortality (Alderson et al 2001). A safe study carried out in 2004 was a RCT of 6997 patient receiving either saline ( Crystalloid) or Albumin (Colloid)showed no difference in 28 day mortality in either group( Fifner et al 4004 ) .
The fluid was administered to frank via central line using alcohol swabs to clean port when accessing lumens to reduce risk of line contamination.(CDC guidelines 2009) The fluid was given at fast rate of 10min. following administration Franks Map had increased to 80mmgh and noradrenaline was weaned done to 14mcg/min. Research supporting the speed of fluid administration includes ……….. Limitations with heart failure.
Frank was monitored for signs of fluid overload due to fluid treatment such as increased FIO2 requirements, increased

On arterial blood gas analysis Frank demonstrated a raised lactate at 2.7. ischemia for unperfused tissue causes a switch to anaerobic metabolism Which leads to Lactic Acid waste This causes decreased ATP to be available for cell work The cell membrane cannot function and it dies This causes release of intracellular enzymes and inflammatory mediators

Frank was receiving Noradrenaline recommended as a first line inotrope for haemodynamic stability al 2009)following fluid ressusitation(Dellinger et Noradrenaline is a inotrope with mainly alpha effects and some beta effects at low doses (Medicines.ie). Noradrenaline is one of the principal neurotransmitters chemical substances involved in the transmission of nerve impulses in the sympathetic nervous system. It is released from nerve cells, and is indicated for the treatment of acute hypotension. The alpha receptors are located in in the skin and cause vasoconstriction thus increasing systemic vascular resistance and increasing blood pressure. (Urden 2007)

(Morton 2005) states that the nurse should be aware of noradrenalines adverse effect of tissue necrosis due to a reduced blood supply to the peripheries. Noradrenaline was administered via a central line as per policy due to the effects and risk of necrosis on smaller peripheral veins with extravasation.

Accurate monitoring of Franks fluid balance and Observations was essential to ascertain effect of treatment. ABG displayed a decreased lactate level of 2.5 mmol. The decision was made to resume maintenance fluid at 15omls per hr. in order to replace the fluid loss from Frank’s drains400mls of serous fluid in a six hour period. Crystalloid fluid was chosen. Two hour late frank remained on 12mcg of noradrenaline to maintain MAP at 65mcg/hr (Dellinger et AL 2008) a further 500mls of colloid fluid was given. Following this the Noradrenaline was decreased to 4mcg/hr. within the next two hours it was discontinued. Map was 68 PAWP was 18mmgh, CVP 12 (PEEP 5)
Copy’’’’Conclusion: Combining physical examinationwith serum bicarbonate and arteriallactate identifies patients with hypoperfusionas defined by low SvO2 andcardiac index. Hypoperfusion may occurdespite supranormal cardiac indices. Patientswith cool extremities and elevatedlactate levels may benefit from a pulmonaryartery catheter to guide but not initiatetherapy.J Trauma. 2001;50:620 –628. Start with a Subjective Assessment of Skin Temperature to Identify Hypoperfusion in Intensive Care Unit PatientsLewis J. Kaplan, MD, Kenneth McPartland, BS, Thomas A. Santora, MD, and Stanley Z. Trooskin, MD

Renal Insufficiency
Acute renal failure is defined as the sudden decline in glomerular filtration (GFR)with subsequent retention of products in the blood that are normally excreted by the kidneys(Urden 2006) Franks reasons for ARF were identified as renal insufficiency related to chronic liver disease compounded by hypovolemic shock intraoperative. The relationship between ARF and chronic liver failure is a complex one and involves vasoconstriction of the renal bed due to inflammation and compounded by abdominal ascites ( betrosian et al 2007). This coupled with hypovolemia due to fluid loss from bleeding due to coagulopathy resulting from liver disease make this patient vulnerable to ARF affecting 18-39% of patients at years 1- respectively and is associated with a high mortality rate without treatment. (Betrosian et al 2007)
Due to this Frank Required Continuous renal replacement therapy(CRRT) via a double lumen vas cath inseted in the right internal jugular vein. The method of CRRT was Continuous veno-venous haemofiltration(CVVH). CVVH removes solutes by convection and ultrafiltration with replacement fluid being used to drive convection. This replacement fluid is adapted to patients specific needs. Lactate free, potassium free, or containing potassium bags are used. (Dirkes and hodge 2007)This mode of CRRT allows for removal of a wide range of solutes across the semipermeable membrane of the filter and is also thought to remove some cytokines with improved patient outcomes thought this remains a controversial topic. Cytokine removal was found to be highest during the first hour of use of a new filter, corresponding to approximately 25 to 50% of the cytokine mass presented to the filter in this time period. This resulted in a significant decrease in the serum concentration of all cytokines(De vrise et al 1999).

Other modes of CRRT include CVVHDF, CVVHD and SCUF. In CVVHDF middle –molecular weight molecules and smaller solutes are removed by diffusion and convection and ultrafiltration . This mode was used traditionally when the ability to replace large amounts of fluid was limited by the technology of the machines (Dirkes and Hodge 2007)
CVVHD uses diffusion snd ultrafiltration. Diffusion in CVVHD does not allow for the removal od larger molecules such as cytokinase (Clark and Belomo 1999) The circuit was primed with heparin with a continuous infusion as per protocol with four hourly APTTs.
CRRT is identified as the preferred mode of Dialysis in critically ill patients and offers gentle treatment and removal of solutes, fluid and possible cytokine and septic mediators ( Ronco and Belomo 2007)
The mode of CRRT chosen for Frank as CVVH was used as small medium and large molecules are removed by convection and ultrafiltation providing
Disadvantages od CRRT include hypothermia due to the removal of blood to and extracorpeal circuit . Franks temperature was 35.1. a Bare hugger warming blanket was applied to maintain teperatur above 36. And reduce risk of associated complications such as limb ischemia, coaglapathy, Arythmia and discomfort and anxiety related to shivering (Jones 2004). Regular limb observations were preformed to ensure skin integrity was preserved. It is important to observe the patient for signs of infection such as raised WBC as this cooling may mask a hyper thermic response to infection (Dirkes and Hodge 2007)Franks WBC were 12.1 (normal range 5-11)
The use of intravenous fluid warmers have been shown in a uni center RCT to have no effect on incidence of hypothermia (Rickard et al 2004)

The risk involved in using heparin to maintain patency of the CRRT circuit is bleeding and the risk of developing Heparin induced thrombocytopenia. Frank as a liver recipient was suseptable to coaglapathy already. In his case heparin was still used despite a raised INr and increased risk of bleeding, This was in order to treat his hepatic artey thrombosis.
Although, as Shown by Aarwal et al 2009 in a study of 50 patient including liver failurepatients, liver transplant recipients with sepis patients used as control group despite having thrombocytopenia and clotting abnormalities circuit life without coagulation was short. They recommend anticoagulation in liver failure patients with repeated circuit clotting with no increased risk of bleeding identified.
The use of citrate is becoming increasingly popular and supported by studies by….. this offers increased circuit life while not systemically anti coagulating patients. Conclusion
Premature clotting of the CRRT circuit increases blood loss, workload, and costs. Circuit patency can be increased. Nonanticoagulation measures include optimization of vascular access (inner diameter, pattern of flow, and position), CRRT settings (partial predilution and individualized control of filtration fraction), and the training of nurses. Systemic anticoagulation interferes with plasmatic coagulation, platelet activation, or both and should be kept at a low dose to mitigate bleeding complications. Regional anticoagulation with citrate emerges as the most promising method.
(Clinical review: Patency of the circuit in continuous renalreplacement therapy
Michael Joannidis1 and Heleen M Oudemans-van Straaten Critical Care 2007, 11:218).
Franks INR was 2.0, Platlets were 32 .It was deceided that the rapid infuser must be removed. In order to do this safely and reduce risk of haemorage from the large insertion site of the rapid infuser, tha heparin in the CRRT was stopped following consultation with the liver surgeons and the intensivists. After four hours the coagulation was checked again as the half life of heparin is four hours.

The use of central lines creates an entry point for bacteria to enter the blood steam and can result in catherrelated blood stream infections. To reduce the risk of the asepsis is required in the insertion, clening and acssesing of all central venous devices. (CDC 2009) . the dressing to Franks Vascath was cleaned with 2% chlorihexidine and a transparent dressing applied to allow for observetion of the site for infection or bleeding .the dressing is changed every 72hrs (CDC guideline 2009)
Frank received an exchange rate of 35mls/kg as recommended by ronco and belomo 2000 . Evidence report adequate clearance at 25mls/kg which reduces patient exposure to hypophosphatemia, cost of replacement fluids and reduces workload with no effect on 90 day mortality of patients on lower exchange rates . (RENAL study 2009)A higher rate of phosphatemia was found in the higher exchange rate group. Franks serum Phosphate level on the lab report was 0.78 and replaced with 40mmol sodium phosphate at 70mls per hr via central line as per policy to maintain phosphate above 1.00.Phosphate is required for the production of ATP and red blood cells and is required for the transport of oxygen. (Urden 2006)
On current evidence at least 70–80% of transplant recipients can be extubated immediately following surgery.

EVALUATION
Folowing correction of fluid ressusitation with a combination of colloid and crystalloid fluids Franks Noradrenaline requirements decreased and by afternoon it was no longer reuired. His ventilator support remained minimal and he was extubated. By the end of shift he remained slightly confused GCS 11/15 and denied pain. He was mainataning a Map of above 65mmgh with crystalloid maintainance fluids at 100mls/hr.

Changes to treatment
- Early extubation
- Citrate versus heparin
- Exchange rate of dialasis
- Family support

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