Senior Nurses Any Insight Into This Patient Case?

Perhaps some more experienced nurses can help me out.

So last shift I had a 60 yr old GI bleeder. PMH of liver CA, renal insufficiency and came to hospital c/o weakness. H&H of 6/18. Potassium of 8. Was to receive 2 units PRBC and insulin, dextrose and bicarb for elevated potassium. Received first unit of PRBC, I redraw chemistry and cbc. Those came back with potassium of about 7 and H&H of 5/17. Doc doesn't understand why H&H dropped after 1st unit PRBC and decides to gastric lavage him to r/o upper GI bleed, comes out negative. Pt stable as far as VS, says he feels fine just alitte dizzy (also very orthostatic) but doesn't look comfortable, sort of sob in our opinions, but pt still says he feels ok. Pt ask to use restroom. Curious I examine the stool, and it's it a large bm of dark red stool.

Doc orders

Lasix 100mg IVP: which I question, I knew he would be getting a few units of PRBC's and they didn't want to overload him, but the patient also had history of renal insufficiency, although he put out about 1200ml of urine. I consult another physician who says because of RI 100mg of lasix would'nt do anything for him anyway and it's no problem to give that much. I; still uncomfortable convince the doc to split the lasix half and half. 50mg IVP after 1st unit PRBC and 50mg later.

Octreotide (sandostatin) drip 25mcg/hr: I see this this ordered with bad GI bleeds. Usually I see a protonix drip (which personally I don't think does anything for our GI bleeders) I wasn't sure what the octreotide would do?

DDAVP (desmopressin) 2mcg SQ : Completely surprised by this order. I ask doc to explain his reasoning for it. He says it's related to platelet function, and can be of some benefit for certain platelet disorders. Although my patient didn't have a platelet disorder I suspect it may have been to put a damper on the bleeding?

I also had to give him the potassium lowering coctail (as I call it) insulin, dextrose, calcium gluconate, bicarb about 3 times as his potassium wasn't coming down obviously due to the continuous GI bleeding.

Finally after hours of the ICU resident scratching his head wondering what was going on/unable to get to bottom of case, he accepted patient to MICU. I sorta wish I pushed the resident to accept the patient sooner, but at my hospital they love keeping patients as ICU evals just to see if their labs/condition stablize then downgrade them hours later. *sigh*

Any insight?





High potassium could be due to the renal insufficiency, or was he on potassium supplements at home and not feeling well, not eating/drinking and was dehydrated. H&H drop, was he being given any IV fluids prior to receiving blood. His original H&H may have been the result of dehydration and when rehydrated that number would be expected to drop. At any rate this is one really sick patient. GI bleeders always scared me, especially the ones who had esophageal bleeds.

Thanks for the input!No I don't think he was given any fluids. I believe because he wasn't tachy or hypotensive also with Renal insuff they probably didn't think fluids was the best treatment at the time. He was a true GI bleed and his low H&H was definitely due to the continous bleeding. Yes the RI could also explain the high K+ but doesn't hemolysis (in GI bleed) also raise K+? The docs kept talking about him getting dialyzed but I think they opted against it and just hoped the K+ would come down with the calcium gluconate and insulin, although after giving him the insulin etc... three times over a period of say 5 hours it wasn't moving his K+ down like it should've. They didn't want to give him kayexylate (for obvious reasons) so idk what they did with him after he went to the ICU. I'll ask the resident next time I see him, maybe he had to get dialyzed after all. I've had all lower GI bleeders. I haven't had any bad upper GI bleeders. Well there was this one lady with chronic alcoholism that came in for vomiting, she was vomiting bright red blood, but she stopped after some time. I had a really bad, and I mean really bad vaginal bleeder about a week ago. I'll post that as a seperate thread.

Multisystem comorbidities. Lots of missing info, such as the cause of his renal insufficiency...there are many, many causes that affect the glomeruli differently in how and what they excrete or retain. Remember, renal insufficiency is not end stage renal disease. The kidneys are still functioning, but how much and in what capacity is unique to the patient's underlying disease. An acute renal failure on top of chronic insufficiency presentation such as your patient, can be caused by multiple factors such as systemic or respiratory infections, endocarditis, drugs such as NSAIDS or volume depletion to name but a few. Large dose lasix is very common in "acute on chronic" renal failure. Depending on the nature of his renal insult, it may also help in potassium wasting. His probable poorly functioning liver does nothing to help matters either, on many levels. Hepatorenal Syndrome comes to mind as well. Very possible if your patient had a cirrhotic liver and ascites. To the best of my knowledge, desmopressin is a hormone that has a secondary use to aid platelet function.Also realize that renal disease in the context of any systemic inflammatory response, even stress, can cause rapid death of red blood cells which if your patient was not losing large volumes of blood and was not volume overloaded, can easily present with a rapidly falling H/H. The rapid cell death will also screw with the potassium. A patient with renal failure has an expected RBC life of only 57 days as it is! (normal RBC life is 120 days).

High potassium levels, or hyperkalemia, has two causes. It can be caused by the body getting too much potassium, in food or medication, or the body releasing too much potassium into the blood stream. There are several reasons why blood cells may give up their potassium. When there is tissue trauma, such as burning, gastrointestinal bleeding, surgery, traumatic injury, or rhabdomyolysis, cells will release potassium into the blood steam. In most cases, tissue trauma isn't sufficient to cause high potassium levels on its own. Usually there is poor kidney function, a shortage of the hormone aldosterone, or increased potassium intake in addition to tissue trauma. The K+ would continue to stay elevated in the presence of continued GI bleed.What Causes High Potassium In The Body? | LIVESTRONG.COMThe patient with a questionable GI bleed should have been on guaiac (hemoccult) all stools for occult blood anyway, but with red blood stool it's apparent that they would be positive. The H/H of 18/6 should have bought him a unit be for obs in the beginning. The H/H can continue to drop while being transfused when the bleed exceeds the transfusion amount and rate. That's how people die from hemorrhage everyday when being massively transfused even with a level one infuser....like a ruptured AAA. Not wanting to use Kayexalate is a good idea in the presence of GI bleed.His renal insufficiency could be due to The GI bleed itself. OR the renal insufficency cause the GI bleed. Gastrointestinal bleeding is a known complication of renal failure; however, its pathogenesis remains uncertain. Some have attributed gastrointestinal bleeding to the effects of uremia on the gastrointestinal mucosa; others have suggested that uremia may affect platelet adhesiveness, which may explain the prolonged gastrointestinal bleeding seen in patients with renal failure.Medscape: Medscape Access requires registration but it's FREE and a valuable resource!!SANDOSTATIN (a synthetic analog of somatostatin, which may also be used) should be given. Octreotide increases splanchnic vascular resistance by inhibiting the release of splanchnic vasodilation hormones (eg, glucagon, vasoactive intestinal peptide). The usual dose is a 50 μg IV bolus, followed by infusion of 50 μg/h. is preferred over previously used agents such as vasopressin PITRESSIN and terlipressin, because it has fewer adverse effects.http://www.bing.com/health/article/g...vt=sandostatinProtonix Pantoprazole (sold under various brand names including Somac, Pantoloc, Protium, Pantecta, Protonix, and Pantoheal) is a proton pump inhibitor drug that inhibits gastric acid secretion and has NO EFFECT on the coagulopathy itself.Octreotide: Drug Information Provided by Lexi-Comp: Merck Manual ProfessionalThe DDAVP would be an agent used in uremic patients with active bleeding is desmopressin (1-deamino-8-D-arginine vasopressin [DDAVP]). It is predominately used to treat diabetes insipidus, mild type I von Willebrand's disease, and bleeding associated with hemophilia A. The mechanism of action of DDAVP has not been fully elucidated, but it is believed to exert part of its hemostatic effect by releasing factor VIII from storage sites, potentially increasing the concentration of factor VIII and minimizing the effects of dysfunctional vWF. It has been shown thatlarger vWF-factor-VIII multimers are present in the plasma after infusion of DDAVP, which might reduce bleeding time. Although the clinical effect of larger vWF-factor-VIII multimers is not well known, there is a strong association between their presence and shortening of bleeding time with the use of DDAVP.I, too, would have used the lasix with extreme caution in the presence of the patient being symptomatic with hypovolemia with dizziness and positive orthostatics for fear of causing the patient to become hypotensive and precipitating shock. Maybe the MD thought that maybe diuresing would help lower the K+ in in the absence of any heart failure.Not knowing any other HX this is the best explanation I can give....I hope it helped.

Quote from All4NursingRNSo last shift I had a 60 yr old GI bleeder. PMH of liver CA, renal insufficiency and came to hospital c/o weakness. H&H of 6/18. Potassium of 8. Was to receive 2 units PRBC and insulin, dextrose and bicarb for elevated potassium. Received first unit of PRBC, I redraw chemistry and cbc. Those came back with potassium of about 7 and H&H of 5/17. Doc doesn't understand why H&H dropped after 1st unit PRBC and decides to gastric lavage him to r/o upper GI bleed, comes out negative. Pt stable as far as VS, says he feels fine just alitte dizzy (also very orthostatic) but doesn't look comfortable, sort of sob in our opinions, but pt still says he feels ok. Pt ask to use restroom. Curious I examine the stool, and it's it a large bm of dark red stool.

Also the patient was recieving duoneb nebulizers. Was this to lower the K+? I cannot remember the renal labs off the top of my head.

Duoneb is a combination product (Albuterol + Ipratropium). Albuterol is a beta agonist that can increase plasma insulin concentration and is sometimes used in hyperkalemia. The thought is the increased insulin release will aid in shifting potassium ions into the intracellular space decreasing levels in the serum. It is another temporizing measure because once the effect of Albuterol is gone, serum potassium will rise again unless the underlying cause of hyperkalemia is eliminated.

oh, man, i love this stuff.

GrnTea, me too. Especially swooning over the detailed pharm/pathophys explanations. OP, was this in the ED or on the floor?

The patient has MANY system failures going on.. the ATTENDING physician needed to consulthematology and oncology.This is NOT for any resident to even considering managing.I would have no qualms telling the ATTENDING physician (the one who makes the most money and is ultimately responsible) THAT!

What were the BUN and Creatinine?

so, op, you are a relatively new nurse? on the floor? must have been a crazy day for you! sounds like you did well! good job. this pt should have been admitted right to a unit.i see a lot of good info already. hepatorenal came to my mind also. the bicarb-insulin-d50-ca++ cocktail is great but usually works best with kayexelate (contraindications already mentioned) since the k that was shifted out of serum shifts back. any ectopy? the pt was on tele? a dialysis run seems warranted to me with that refractory k. i see this pt being admitted to the unit under an intensivist, ffp given, egd at bedside asap, prbc running (in the icu, we can run these products much faster)to reinforce and speculate-octreotide drip- yes!- lets clamp up the blood flow to slow the bleedpantoprazole drip- we can use both!- the body is in a stress state, likely hyper-secretory, lets nip that in the gluteus ddavp- maybe something they pulled out of the heme-onc history? i'm not an onco person at all. some day i'll work that department to brush up! i have used ddavp in di, von willebrand's (pre- and post- elective sx), and ttp/itp. all those patients were in the peds population. is it possible that we are adding in lasix as prophylaxis for the fluid retention/hyponatremia/chf that could develop when this is given to a renal pt? ensure the med is excreted by the kidneys in a timely fashion? dump k+? also, the ddavp would assist the octreotide in vasoconstriction of splanchnic flow, would it not? (highlighted because i want feedback!)you remembered a lot. i am curious about the rest of the chem- bun/creat, na, co2 (bicarb) but that's ok. i also wonder about coags and plt count (sounds like you remember plt as wnl, though)maybe i'll think about this more? i love armchair medicine!