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Group 5: Julia Bernas, Stephanie Bevivino, Stephen Dias, Johnny Lavinio, Lindsay Worthmann Patient: Gary Rosenfeld (M) November 12, 2015Problem List:Hyperkalemia, diabetic foot infection, hyperglycemia/uncontrolled T2DM, maintenance management of T2DM, and obesity.Assessment:The first problem GR presents with today is acute hyperkalemia as evidenced by the elevated potassium level of 7 mEq/L and abnormal ECG reading with peaked T waves and a rate of 110 bpm. While CKD and some medications (ACEIs, ARBs, potassium-sparing diuretics) are common causes of hyperkalemia, GR does not currently present with any of these issues. Rather, his history of T2DM is likely the cause. The 2014 Clinical Practice Guidelines for the Treatment of Acute Hyperkalemia in Adults brings out that the most severe potential outcome of hyperkalemia is the development of cardiac arrhythmias leading to cardiac arrest.1 Therefore, goals of therapy for GR will include decreasing potassium to the normal levels of 3.5-5.0 mmol/L to prevent serious cardiac complications, limiting adverse effects of treatments such as hypervolemia, alkalosis, or hypernatremia, and preventing recurrence of this electrolyte disorder. In order to best protect the heart from serious damage, the guidelines recommend immediate IV calcium salts (either calcium chloride (10%) 500-1000 mg (5-10 mL) IV over 2-5 mins or calcium gluconate (10%) 1500-3000 mg IV over 2-5 mins).1,2 Administration of IV calcium helps stabilize the cardiac membrane and lessens the likelihood that an arrhythmia will occur. IV calcium works in as little as three minutes (improvements identified on ECG), but due to its short duration of action (30-60 minutes), future doses may be necessary if the hyperkalemia is unable to be resolved.1 Calcium chloride may be preferred over calcium gluconate due to it providing three times the amount of calcium and potentially being more bioavailable (resulting in fewer doses needed) as long as extravasation is closely monitored.1 IV calcium does not cause excretion of K from the body, so added therapy is needed in order to reduce the K levels back within the normal range. It is recommended that 10 units of regular insulin be administered over 15-30 minutes so as to activate the body’s Na+/K+ ATPase pump to increase the cellular uptake of K1,2. Administering insulin alone can lead to hypoglycemia, so it is suggested to deliver the insulin with D50 (25 g, or 50 mL) if the BG is less than 250 mg/dL.1 However, GR has a BG of 300 mg/dL, so D50 is not necessary at this time. Other possible medications that can be used to shift the K intracellularly if the insulin is not effective are sodium bicarbonate 50 mEq IV over 5 minutes or a nebulized beta-agonist (albuterol) at a dose of 10-20 mg over 15 minutes.1,2 Sodium bicarbonate seems to be least effective of these three at shifting the K inside the cells and also has the highest risk for side effects and therefore is not commonly utilized.1Another tactic that can be used to treat hyperkalemia is increasing the renal excretion of K. The use of diuretics, K-binding resins, or dialysis are ways in which this can be achieved.2 Sodium polystyrene sulfonate is the common K-binding resin administered at a dose of 15g po 1-4 times/day or 30-50 g q6h rectally.2 While effective, a diuretic may not be ideal due to greater risks of dehydration. Therefore, the use of a potassium-binding resin would likely be a better option for this patient in managing his longer-term K levels. The second problem for GR is his presentation of a DFI. He has known of the wound for about two months, but has not sought medical attention until now. He has not changed his socks for several weeks, and when they were cut off in the ED, his third toe was necrotic and fell off during his foot exam. Maggots were present in the wound between his big toe (which also has an ingrown toenail) and second toe, which tracts to the bone on palpation. The entire foot has 2+ edema, erythema, and is warm to touch. GR has no sensation in his foot and has wounds and small lacerations covering the entire heel, arch, and pad. Also, GR demonstrates signs of infection (swelling, erythema, local warmth, and purulent discharge), he meets SIRS criteria (temp of 100.9F (38.2C > 38) and WBC of 16 (>12)), making it evident that this is a severe case of DFI.3 The lost toe was sent for culture, and results show Gram (+) cocci and Gram (-) rods. Goals of therapy for GR’s DFI will involve preventing/minimizing osteomyelitis or the need for surgery, optimally treating and ridding the infection, improving the condition of his wound, and ultimately improving his quality of life. The wound first needs to be cleaned, debrided, and appropriately dressed to promote healing as recommended by the 2012 IDSA Clinical Practice Guidelines for the Diagnosis and Treatment of Diabetic Foot Infections. The limb should be elevated to decrease edema and provide necessary pressure relief.3 In addition to these non-pharmacological methods, the use of a broad-spectrum empiric antibiotic therapy that contains coverage against GPC, as well as gram-negative and obligate anaerobic organisms to treat severe infections is suggested.3 Since this is a severe infection, it is recommended to begin with IV therapy before switching over to a PO agent once clinical response is seen.3The following antibiotic combinations(mentioned in the guidelines) will cover the GPC and gram(-) organisms: ampicillin/sulbactam and vancomycin, piperacillin/tazobactam and vancomycin, clindamycin and ceftazidime or cefepime, linezolid and piperacillin/tazobactam, or vancomycin and a carbapenem.3 While each of these are potential options, there is an increasing prevalence MRSA with DFI.3 GR may also be at an increased risk for MRSA due to leaving his wound untreated for upwards of 2 mo. The IDSA guidelines recommend empirically treating DFI patients with antibiotics that have activity against MRSA when the infection is severe enough that not guarding against MRSA (while cultures are still being obtained) would present too high of a risk of treatment failure.3 Out of the listed antibiotic options, vancomycin (15-20 mg/kg q8-12h) is most commonly used for MRSA coverage. Fluoroquinolones are sometimes viewed as an option for treating DFI, but they have suboptimal coverage against S. aureus, making them an invalid option for GR. Early gen. cephalosporins will cover MSSA, but only ceftaroline (5th gen.) is able to treat MRSA, as well as gram (-) organisms. Given that piperacillin/tazobactam (3.375 g every 6 hours for 7-10 days) has better coverage of gram (-) than ampicillin/sulbactam (including pseudomonas), this is viewed as a better option to be paired with vancomycin in the case of GR. This combination should best allow for the coverage of MRSA as well as the most extensive coverage for the strains of bacteria known to be present. Per the IDSA guidelines, treatment for severe infections should last 2-3 wks.3 It is recommended to treat until s/sx have been eliminated, not necessarily until complete healing of the wound is achieved.3 Close attention should be paid to the patient’s s/sx, and overall condition throughout his course of therapy in order to evaluate the possibility of transition from IV therapy to oral, as suggested by the guidelines.3Due to the necrotic nature of GRs foot/toes, the guidelines suggest that an MRI be done to evaluate for the potential of osteomyelitis.3 The possibility of surgery is greater in patients with this condition and thus, a surgeon should be involved in the evaluation of the patient.3 If the MRI comes back positive for osteomyelitis, antibiotic therapy may need to be reevaluated and even extended out for a longer period of time.3 If the hospital chooses to use contrast dye for the MRI, metformin should be discontinued 48 hours before the procedure to prevent the formation of lactic acidosis.4 GR’s third problem is his presentation with hyperglycemia secondary to uncontrolled T2DM as evidenced by his complaints of polyuria, polydipsia, and polyphagia, BG of 300 mg/dL, and A1C 12.2%. Patient also presents with no sensation in his affected foot. GR does not present with SOB, CP, blurred vision, or retinopathy and SCr and CrCl are normal. Goals of therapy include effectively decreasing BG to an inpatient goal of less than 140 mg/dL, relieving s/sx associated with hyperglycemia, preventing harmful effects of hyperglycemia (namely, neuropathy, nephropathy, and retinopathy), avoiding recurrence of hyperglycemia by maintaining BG at a level of 70-140 mg/dL while inpatient, and improving quality of life.5 Hospital protocol recommends administering insulin at a basal dose of NPH 0.1units/kg (actual BW) SQ BID. A nutritional dose is also recommended to be administered with the NPH and should be dosed by dividing the daily NPH dose by 6 and given before breakfast and dinner. If necessary after BG levels have been adjusted, a correctional dose of regular insulin can be given with the basal and nutritional insulin depending on BG levels. Hospital protocol recommends that with BG 151-200, give 2 units of regular insulin; with BG 201-250, give 4 units; with BG 251-300, give 6 units; with BG 301-350, give 8 units; and with BG 351-400 units, give 10 units and call MD. GR is non-ICU, so insulin can be given SQ. While inpatient and receiving insulin, metformin should be discontinued. Upon discharge, maintenance treatment of T2DM should be reevaluated.Plan:Proper cleansing, dressing, and care of foot wounds, as well as elevation and immobility of lower limb. Administer 10 mL calcium chloride 10% IV push slowly over 10 minutes x1Administer 10 units regular insulin IV push x1Albuterol sulfate 2.5ml/0.5ml vials - 2 mL inhaled via nebulizerAdminister sodium polystyrene sulfonate 15 gm suspension PO Q6h until serum K reaches 5 mEq/L or lowerVancomycin IV 1500mg Q12h over 90 min AND piperacillin/tazobactam 3.375g Q6h over 30 min up to 4 weeks depending on clinical response (consider de-escalation of abx therapy once susceptibilities are found and organisms identified)D/C Metformin while inpatientAdminister NPH 10 units SQ BID before breakfast and dinner AND regular insulin 3 units SQ BID before breakfast and dinner (In one syringe). Correctional dosing if necessary depending on response to initial insulin dosingMonitor CHEM7 at 1, 2, 4, 6, and 24h, and continuous 3-lead ECG monitoring throughout treatment of hyperkalemiaMonitor for signs of extravasation and tissue necrosis due to calcium chlorideMonitor for signs of systemic and/or worsening infection (CBC, BP, P, Temp, RR, erythema, edema, pus on wounds, healing of wounds)Send patient for MRI once stable and 48 hours have passed since metformin D/C (if contrast dye used), and request a consult with a surgeon and DFI expert to evaluate need for amputation.Monitor BG to assess proper treatment strategies (before every meal and at bedtime)Counsel patient on the importance of SMBG, daily foot checks/changing socks, hygiene, controlling T2DM to prevent secondary complicationsCounsel patient about insulin possibly causing weight gain, hypoglycemia and injection site rxnsEducate patient on uncontrolled BG levels leading to DFI and emphasize proper glycemic controlReferences:Alfonzo A, Soar J, MacTier R. Clinical Practice Guidelines for the Treatment of Acute Hyperkalemia in Adults. The Renal Association. [Internet] 01 March 2014. [cited 2015 Nov 10] Available from: guidelines. Ecc Committee. (2005). Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. [Internet] Circulation,112(24 Suppl), 1-203. [cited 2015 Nov 10] 10.1 Life-Threatening Electrolyte Abnormalities. Available from: . Lipsky B, Berendt A, Cornia P, et al. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. [Internet]Clinical infectious diseases 54.12 (2012): [cited 2015 Nov 10] e132-e173.Available from: Rasuli P, Hammond I. Metformin and contrast media: where is the conflict?. [Internet] Can Assoc Radiol J 49(3), 161.[cited 2015 Nov 10] Available from: V, Johnston J. Inpatient management of hyperglycemia and diabetes. [Internet] Clin Dia. 29(1), 3. [cited 2015 Nov 10] Available from: ................
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