Monday, April 30, 2012
Saturday, April 28, 2012
As I sat reviewing the chart my attending posed the following question "So is it reasonable to continue PD here in the unit or should we switch over to HD until she's extubated and clinically improving?"
Would the increased intra-abdominal pressure from PD lead to prolonged intubation time? Given the manipulation of the thoracic cavity was there a higher risk of dialysate leak through the diaphragm? Would we be able to provide adequate clearance and ultrafiltration with PD? Would the infection risk be higher for PD given the relative unfamiliarity of the nursing staff?
A recent article in Peritoneal Dialysis International comparing perioperative outcomes in patients on PD and HD post cardiac surgery sheds some light on the situation. In the study the Southern California Permanente Group at Los Angeles Medical Center looked back at 15 years of CABG and cardiac valve replacement surgeries in ESRD patients and compared a variety of outcomes between 36 patients on PD and 76 on HD.
There were no reported significant differences between the two groups at baseline including age, dialysis vintage, presence of diabetes, type of surgery and Charlson comorbidity index. The only statistically significant difference in terms of outcomes was a slightly longer median length of stay in the cardiac surgical unit for HD patients (4 vs 2 days) though the median total hospital length of stay between the two groups was no different (PD 9.5 days, HD 10 days).
There was trend towards more infections in the HD group (19% vs 6%) but this did not reach statistical significance. Median intubation time was the same between groups. Survival perioperatively (defined as during the hospital stay or within 30 days of operation) and at one and two years was similar between groups (PD 89%, 81%, 69%, HD 90%, 78%, 66%).
Conversion of PD patients to HD occurred in just 6% percent of patients. One for dialysate leak and another for uncontrolled azotemia. CRRT was needed in 1 HD patient due to hemodynamic instability.
The study doesn't answer the question of whether converting a patient on PD to HD or CRRT might improve outcomes but it does provide reassurance that PD patients don't have an excessive risk of dialysate leak or inability to achieve adequate clearance and ultrafiltration. It also shows that in general outcomes post cardiac surgery between PD and HD patients are similar.
In our patient we continued peritoneal dialysis using an automated cycler without difficulty. Over the weekend the covering team changed to HD via the arteriovenous graft over concern that PD might lead to a dialysate leak. Unfortunately the patient tolerated HD poorly with episodes of hypotension so we transitioned back to PD when we came back on. The rest of her hospitalization was without incident.
Thursday, April 26, 2012
Thursday, April 19, 2012
A 41 year old gentleman with no past medical history presented to ER for nausea, vomiting and abdominal pain.
The commonest causes of renal infarcts are emboli from atrial fibrillation, infective endocarditis, or fat, renal artery or aortic dissection, fibromuscular dysplasia and vasculitis. Work-up including an EKG, ECHO, hypercoagulable panel and antiphospholipid antibodies were all negative. We performed an angiogram which showed diffuse visceral microaneurysms leading to a diagnosis of polyarteritis nodosa.
Polyarteritis nodosa (PAN) is a systemic necrotizing vasculitis that affects medium sized vessels. It was first described by Dr. Kussmaul and Dr. Maier in 1866. The incidence of the disease is 2 to 33 per million population, with a male to female ratio of 1.5:1. The major environment factor associated with PAN is HBV infection.
There are 5 variables that predict an increased risk of mortality in PAN (Five factors score FSS): 1) Proteinuria>1g/day
2) Renal insufficiency (Cr>1.58)
3) GI involvement (bleeding perforation, infarction or pancreatitis)
5) Central venous system involvement.
Without treatment, the 5 year mortality in patients with 0 risk factor is <12%, 1 risk factor 25% and 2 risk factors 56%. The standard treatment for FSS>1 is 12 months Cytoxan with steroids. Renal failure is rare in PAN patients and uncontrolled or relapsing vasculitis is the most common cause of death.
In our case, the patient was started on cytoxan and prednisone and his abdominal pain completely resolved. His creatinine unfortunately is still elevated and the plan is to continue with treatment for at least 6 months.
Posted by Jie Cui
Saturday, April 14, 2012
If you're interested, check it out here.
Friday, April 13, 2012
Nate Hellman, the founder of this blog, was a personal friend. We trained together as MGH Renal Fellows. It has been three years since his passing. I often wonder how much he would have achieved by now. For sure, he would be on staff at Mass General and on faculty at Harvard Medical School. He would be well immersed in setting up his independent research career. He would be the caring doctor we all knew him to be. And most certainly, he would be writing this blog.
Those of us who knew him personally, know that Nate had the ability to write and release his brilliant thoughts to the world with little worry or inhibition, one of many traits I always admired in him. I think it came from his wonderful ability to laugh at himself and remain honest and real, no matter what. I have decided to start blogging, in an effort to remind myself, all of us here at MGH and all of you out there of “Nate’s method.” At least, I intend to try…
Here is the unknown case that was presented to me at the MGH Renal Grand Rounds this past Tuesday. One of our Renal Fellows, Dr. Jie Cui, presented the case, and will be blogging on her own thoughts on PAN soon (I have inside information here!):
41 yo M with no PMH was admitted with acute onset pain radiating to his R groin, 10/10, sharp and persistent. In the ER, he was found to have BP 188/116, mildly elevated Cr to 1.3, and elevated LDH 520. His CT showed bilateral renal infarcts and renal artery clot.
Home Medication: None
Vital Signs: T 98 HR 76 BP 120/90
GEN: Well appearing man in NAD
HEENT: MMM, oropharynx clear; PERRL.
Cards: NSR, RRR, normal S1, S2, no murmur/gallops/rubs
Chest: CTA B/L, no wheezing/rales/rhonchi
Abd: Soft/ND, + BS, RLQ (+) tenderness, no rebound/guarding, no bruits
Back: no CVA tenderness
Ext: normal tone, no edema, 5/5 muscle strength, no joint tenderness or deformities
Skin: no rash
NA 135, K 3.7, CL 101, CO2 23, BUN 10, CRE 1.42, EGFR 55, GLU 80
CA 8.8, MG 2.3, TBILI 0.5, TP 6.9, ALB 3.5, GLOB 3.4, LDH 363 CRP 11.8
ALT/SGPT 18, AST/SGOT 12, ALKP 73, TBILI 0.5
FE 33, TIBC 194, TIBC 161
WBC 9.84, RBC 3.98, HGB 12.7, HCT 36.1, MCV 90.7, MCH 31.9, MCHC 35.2, PLT 226
PT 14.5, PT-INR 1.1, PTT 59.0,
Hypercoagulable work up (-) antiphospholipid antibodies (-), homocysteine (-)
ANA (-), ANCA (-), C3, C4 normal, Cryo (-),hepatitis (-), HIV (-),
Urine protein/cr: 0.12, 24 hour urine creatinine clearance: 54ml/min
Urine sediment: 1-2 WBC, 1-2 normal RBCs, no casts.
All Cultures were negative.
CT abdomen and pelvis:
1. Bilateral renal artery clot
2. There is a focal, geographic area of decreased perfusion involving the upper pole of the right kidney.
3. A focal area of cortical volume loss and decreased enhancement in the left kidney is also noted, suggestive of scarring.
Questions for the discussant:
1. What is the differential diagnosis?
2. What diagnostic procedure would you perform?
We discussed the following differential:
The differential of acute flank pain is:
Renal calculus – but no evidence on CT
Pyelonephritis – but cultures were negative
Other abdominal pathology as source of the pain – pancreatitis, cholecystitis – but no evidence on CT
Renal Infarct – yes, there is evidence for this on CT
This brings us to the differential for renal infarct:
Thromboembolic – from heart or aorta – but echocardiogram, including transesophageal echo with bubble study were negative, also cultures remained negative at all times
In situ thrombosis – no clear evidence for this
Renal artery occlusion from aortic dissection – no evidence for this on CT
Spontaneous or iatrogenic renal artery dissection – no evidence for this on CT
Fibromuscular dysplasia – no evidence for this based on history (no h/o HTN for example)
Segmental arterial mediolysis – possible, but again not supported by the CT
Complication of anti-phospholopid syndrome – but entire hypercoagulability panel was negative
Cocaine use – this could easily be the cause of this bilateral renal artery thrombosis, the patient continued to deny cocaine use, but this was strongly suspected, urine tox studies were apparently negative, but timing may have been the issue there...
Polyarteritis nodosa – interesting and also likely, the patient is HBV negative, but could be “idiopathic” PAN.
Given the above differential, a renal angiogram was performed which was read as consistent with medium vessel vasculitis, suggestive of PAN.
The patient was treated with steroids and cytoxan and is presently doing well, with creatinine stable in the 1.4 range and no new symptoms.
Still, we were left a bit dissatisfied with this outcome, as the diagnosis of PAN is not consistent with bilateral renal artery clot, which was clearly seen on CT in this patient.
I am still worried about cocaine use or another etiology…
Please comment and let us know your thoughts!