Nursing Care of Crrt Hyovolemia

1 January 2017

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.

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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. f 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.

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).

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