CLINICAL CASE PRESENTATION

Chief Complaint

Disorientation that has progressed during the last 3 days leading to hypoactivity and obduntation.

HPI

Case of 49 y/o male with history of DM 2, HTN and DKA which presented with abdominal pain and vomits (unquantified) that led to anorexia. Progressing weakness and malaise that led to obduntation within 3 days. Denies fevers, night sweats. Nothing seemed to relieve it. Patient with poor compliance to his medications.

H&P

VS:

BP-68/39 P-74
H: 68

R-24

T-36.6
BMI:21.2

Somatometry:

W:125lb

Presents with hypoactivity, dry oral mucosa, generalized abdominal pain. Patient is divorced, accepts transfusions. Heavy equipment driver. PMH:DM2, HTN, MDD. Allergies:NKDA FHx: Diabetes-Mother and Father. HTN-Father. Heart Disease-Father and brother. SHx: None

Admitted

ICU Vs: q 4hrs and chart, Dxt: q 1hr and chart, Foley Catheter. IVFs: 0.9NSS 1000ml full drip then at 150ml/hr. Regular insulin 100U/100ml 0.9NSS to run at 6ml/hr. Rocephin 1gr IV QD. O2 by NC at 3L/min When Dxt <250 switch IV fluids to 0.45NSS/D5W 1000ml to run at 60ml/hr. Labs:CBC+difff, BMP+Ketones q 2hrs x3 then q 4hrs, U/A, U/C, B/C q 15min x3, EKG, Cardiac enzymes, ABG, PT, PTT, INR, CXR.

5-20-13 ABGs

pH 6.935 pC02 17.4 pO2 208 BE - -27.5 HCO3a 3.6 O2 sat 98.4

5-20-13 Labs
CBC WBC 23.6 RBC 3.6 HGB 10.2 HCT 34.7 MCV 99.6 PLT 216 Neut 77 Lymph 11 Mono 10 NRBC 0 Band Creatine Kinase - 595

BMP Glucose 1248 BUN 80 Creatinine 3.91 Sodium 115 Potassium 8.9 Chloride 73 CO2 4 Calcium 9 BUN/Creat Ratio 20.41 Anion Gap with K+ - 46.90

5-20-13 Urinalysis

Glucose >=1000 Bilirubin negative Ketone 15 S. Gravity 1.027 Protein negative pH 5.0 Nitrite negative Blood moderate Leukocytes - negative

RBC 4.1 WBC 5.4 Casts 11.1 Bacteria - loaded

Se reciben los labs ordenados estando en ICU. 5-21-13 ABGs 12:30 AM

pH 7.188 pC02 16.5 pO2 255.2 BE - -19.6 HCO3a 6.1 O2 sat 99.6

5-21-13 12:50 AM Labs

BMP Glucose 910 BUN 77 Creatinine 3.58 Sodium 122 Potassium 6.0 Chloride 84 CO2 5.0 Calcium 8.8 Anion Gap 39.0

5-21-13 ABGs 3:30 AM

pH 7.307 pC02 21.09 pO2 220 BE - -13.3 HCO3a 10.7 O2 sat 99.6

5-21-13 4:38 AM Labs

Neut 86.2 Lymph 10.4 Mono 3.1 NRBC 0 Band CK - 1186 CPK-MB 44.8 Troponin 0.06 TSH 3.62

CBC

WBC 14.1 RBC 3.58

HGB 10.1
HCT 30.9 MCV 86.3 PLT 167

5-21-13 4:38 AM Labs

BMP Glucose 536 BUN 69 Creatinine 2.81 Sodium 130 Potassium 4.2 Chloride 90 CO2 14.0 Calcium 9.2 Anion Gap 30.2

5-21-13 9:33 AM Labs

BMP Glucose 166 BUN 55 Creatinine 1.90 Sodium 136 Potassium 3.4 Chloride 100 CO2 25.0 Calcium 9.2 Anion Gap 14.0

Progress Note

VS- BP:135/73 P:101 R:20 T:36.5 Patient with a WD of 4.86L, lethargic not arousable in metabolic acidosis. Hgb A1c-12.5 Orders:
BMP

stat, Bicarbonate x1, Nephro consult, VM O2 at 50%, Dxt q 1hr, Hgb A1c, EKG.

(5.21.13)

Inputs: 8,689ml/24hrs Output: 2,900ml/24hrs

5-21-13 ABGs 4:00 PM

pH 7.360 pC02 32.2 pO2 124.8 BE - -6.5 HCO3a 17.8 O2 sat 98.5

Nephrology Consult (5/21)

Assesment:
DKA

resolving AKI resolving Hypokalemia start IV replacement.

Orders:
20meq

KCl/500ml 0.45NSS to run in 6hrs x1. BMP after replacement.

5-21-13 4:00 PM AM Labs

BMP Glucose 278 BUN 38 Creatinine 1.42 Sodium 137 Potassium 4.4 Chloride 105 CO2 18 Calcium 8 Anion Gap 18.4

Labs-(5/22/2013) 12:15am

Ketones: small Glc:87 BUN:23 Cr:0.99 Na:142 K:3.5 Cl:111 CO2:25

Ca:7.9 (8.8) BUN/Cr:23.23 GFR: >60

Labs-(5/22/2013) 5:09am

Glc:45 BUN:13 Cr:0.76 Na:141 K:3.0 Cl:110 CO2:25

Ca:7.8 (8.8) Phosphorus: 0.7 Mg:1.76

Amy:238 Lip:163

Labs-(5/22/2013) 11:07am

Glc:71 BUN:8 Cr:0.70 Na:140 K:2.9 Cl:108 CO2:25

Ca: 7.7 BUN/Cr:11.43 Ketones: Moderate

Progress Note (5/22/2013)

VS- BP:145/90 P:94 R: 20 T:37.5 Patient is stable, arousable and responds verbally. Mild abdominal discomfort. Phosphate, Mg and K replacement will ensure. Orders:
KCl 40meq/500ml 0.45%NSS to run in 8hrs x 2. Potassium Phosphate 10meq/250 D5W run in 4hrs x2. Abdomianl sono and ABG BMP when replacement finishes. Decrease Insulin drip to 3ml/hr. Start D10W+ 20meq KCL to run at 60ml/hr. Amilase and lipase.

(5/22/2013)

Inputs: 7119 Outputs: 8000

Labs May 22, 2013

CHEMISTRY GLU BUN CREA NA+ K+ CLCO2 CA++ PO4 MG++ ALB AMYLASE LIPASE KETONES SMALL 12:15 AM 87 23 0.99 142 3.5 111 25 7.9 5:09 AM 45 13 0.76 141 3.0 110 25 7.8 0.7 1.76 2.7 238 163 MODERATE MODERATE 198 117 NEGATIVE 10:23 AM 71 8 0.70 140 2.9 108 25 7.7 11:33 AM 8:04 PM 142 4 0.64 141 3.3 106 27 7.5 NORMAL RANGE 70-99 MG/DL 7-18 MG/DL 0.60-1.00 MG/DL 136-145 MMOL/L 3.5-5.1 MMOL/L 101-106 MMOL/L 24-31 MMOL/L 8.9-9.8 MG/DL 3.0-4.5 MG/DL 1.7-2.8 MG/DL 3.5-4.5 G/DL 28-100 U/L 22-51 U/L NEGATIVE

ABGs May 22, 2013

ABGs pH pCO2 8:05 AM 7.466 34.3 REFERENCE RANGE 7.355-7.475 31.7-46.9 mmHg

pO2
BE HCO3 O2 Sat

100.8
1.1 24.2 98.2

68.8-114.5 mmHg
mmol/L mmol/L %

Labs May 23, 2013

CHEMISTRY GLU BUN CREA NA+ K+ CLCO2 CA++ PO4 MG++ ALB KETONES NEGATIVE 12:05 AM 70 3 0.49 142 3.2 108 29 7.7 1.1 1.41 2.7 SMALL 5:45 AM 221 3 0.58 137 4.0 107 23 7.5 1.7 2:03 PM 54 4 0.58 140 3.5 111 24 7.8 1.6 1.7 2.6 NEGATIVE 8:41 PM 222 6 0.48 133 6.6 105 25 7.3 NORMAL RANGE 70-99 MG/DL 7-18 MG/DL 0.60-1.00 MG/DL 136-145 MMOL/L 3.5-5.1 MMOL/L 101-106 MMOL/L 24-31 MMOL/L 8.9-9.8 MG/DL 3.0-4.5 MG/DL 1.7-2.8 MG/DL 3.5-4.5 G/DL NEGATIVE

Summary of days 5/22/13 and 5/23/13

Management consisted frequent blood sampling to monitor electrolyte and glucose levels while being provided IV insulin and IV hydration. Electrolytes were replaced accordingly as needed, including magnesium and potassium.

Labs (5/22/2013) 9:17pm

Glc:142 BUN:4 Cr:0.64 Na:141 K.3.3 Cl:106 CO2:27 Ca:7.5

Amylase: 198 Lipase: 117

5/24/13
Patient was placed in diabetic diet and Lantus and Humalog insulin were calculated. Further labs were ordered to follow glucose and hyperkalemia. FM: Follow-up glycemic adjustment Follow-up hyperkalemia

5/24/13
Mycelex troche 1 tab PO 5 times daily FM Orders: Lantus and Humalog Diabetic diet Toradol 60mg IM Enalapril Orders: D/C 0.9 NS Increase 0.45 SS to run at 60ml/hr BMP with ketones Amylase and lipase

5/24/13
BMP: 7:52am BMP: 10:32pm
138 | 111 | 7 / 62 4.1 | 25 | 0.48 \ Anion Gap w/ K 6.10 Ketones small Amylase 59 U/L 136 | 106 | 10 / 212 5.0 | 26 | 0.55 \ Anion Gap w/ K 9.0

Lipase 51 U/L

5/25/13

FM- transfer to medicine ward

5/25/13
FM Orders: Increase Lantus to 36 U SC daily at 9:00pm Orders: Restoril 30 mg PO AS

5/25/13
BMP:
133 | 102 | 12 / 296 4.3 | 25 |0.65 \ Anion Gap w/ K 10.30

26/May/13
Labs

Vitals
Bp:

CBC
WBC:

147/80 HR: 83 RR 20 T:36.8

10.9 N: 60.4% Hgb: 13.1

Dextro 224mg/dl

27/may/13

Vitals
139/73 HR: 87 RR: 20 T: 36.7 Dextro am: 301mg/dl
BP:

BMP
Gluc:

Tolerating regular diabetic diet, insulin cover is evaluated.

309mg/dL BUN: 12mg/dL Creat: 0.96 mg/dL Na+: 135 mmol/L K+: 4.5 mmol/L CO2: 27 mmol/L Anion gap: 17.5mmol/L

May 27, 2013

Patient will be discharged home with home IV insulin therapy tailored to his needs.

DIABETIC KETOACIDOSIS

Intro

Part of the hyperglycemia spectrum:

DKA
HHS

Typically presents on DM1(de novo), but occurs on DM2 on the following conditions:
Serious Trauma

Infx (Pneumonia, AGE, UTI) 40-50%

Cardiovascular(MI)
Stress

(Stroke, pancreatitis, drugs, EtOH)

Intro

More common in woman and young(<65) males. Mortality is primarily due to primary underlying illness, and this increases at the extremes of age and in presence in coma or hypotension.

Pathogenesis

Two mayor hormonal abnormalities:

Insulin

deficiency and/or resistance. Glucagon excess

Aditionally
Increased

catecholamines and cortisol secretion.

All this adds up to elevated glucose concentrations:

HHS:

1000mg/dL DKA: Usually <800mg/dL

Definitions

HHS- Ketoacids little or not present (serum and urine), plasma osmolality may reach 380mosml, neuro abnormalities (25-50%). pH>7.30, serum bicarb >20meq/L, serum Glc>600. DKA- Triada (Hiperglicemia, AG Met Acidosis, ketonemia) Glc-500/800, exceptions like: starvation, pregnancy or insulin tx before evaluations may have lower dxt.

Clinical presentation

DKA evolution is quick. Initially hyperventilation and abdominal pain. Can expect hyperglicemia symptoms: polyuria, polydipsia and weightloss. Neuro symptoms (osml >320-330) depending of the degree or duration of the hyperglicemia (lethargy, focal signs like hemianopsia hemiparesis, obtundation) can progress to coma.

Clinical Presentation

Abdominal Pain- correlates to the degree of metabolic acidosis, serum bicarbonate <5meq/L (85%) and >15meq/L (13%). Kussmaul respirations with fruity odor. Fever if the source is infection.

Labs

Acute BUN and Creatinine serum levels (induced by decreased GFR induced by hypovolemia). What to order?
Serum glucose Serum electrolytes (with calculation of the anion gap) drop in Na aprox. 1:62(<400mg/dL) 1:42 ( for q 100meq above 100) Complete blood count with differential Urinalysis, and urine ketones by dipstick Plasma osmolality

Effective Posm = [2 x Na (meq/L)] + [glucose (mg/dL) 18]

Serum ketones (if urine ketones are present) ABG (if urine ketones or anion gap are present)

Differential Diagnosis

Alcoholic and fasting ketoacidosis: Serum bicarb usually >14 meq/L. Low carb diets. Other high anion gap met.acidosis. (MUDPILES).

Additional Labs

U/C Sputum/C B/C Serum lipase and amylase CXR Measurement of A1C

Approach

Its a medical emergency! H&P Evaluate:

Airway,

breathing, and circulation (ABC) status Mental status Possible precipitating events ( source of infection, myocardial infarction) Volume status (Body Water Deficit (in liters) = ( 0.6 * Wt * [(Na/140) - 1] )

Treatment

Normalize the AG. (Correcting the acidosis). Fluid replacement goals.

Reexpand

the intravascular volume. Restore renal perfusion. Aprox loss of 70meq of Na and K for each liter.

Avoid cerebral edema with rapid repletion.

Fluid repletion

Initially with 0.9% NSS this will:

Replace

fluid deficit. Quicker than 0.45% to correct extracellular volume. Lower plasma osmolality ( it is hypoosmotic for this patients) Decreased glucose levels by dilution and urinary losses (renal perfusion is increased)

Fluid repletion

No cardiac compromise: 10-15ml/kg per hour during the first hours. (Max 50ml/kg in 4 hours) Most patients are switched at some point to 0.45% NSS to replace the free water loss induced by the glucose osmotic diuresis, there are concerns about the possible development of cerebral edema if the plasma osmolality is reduced too rapidly. Fluid repletion can initially reduce the serum glucose by 35 to 70 mg/dL per hour due to both hemodilution and increased urinary losses as renal perfusion is enhanced.

Fluid Replacement (K)

Patients with an initial serum potassium below 3.3 meq/L should receive aggressive fluid and potassium replacement PRIOR to treatment with insulin. Due to shift of potassium out of the cells due primarily to insulin deficiency and hyperosmolality, K is often elevated at presentation. In such patients, potassium repletion is not begun until the serum potassium concentration falls below 5.3 meq/L. If 40 meq of potassium is added to each liter, 0.45% NSS should be used if the patient is hemodynamically stable since this solution contains 77 meq of sodium and 40 meq of potassium so is equivalent to approximately .75% isotonic saline. If the addition of K to 0.9%NSS results in the generation of a hypertonic fluid that will not correct the hyperosmolality.

Insulin Therapy

DKA can be treated either with an IV bolus (0.1 U/kg body weight), followed by a continuous infusion of regular insulin at a dose of 0.1 U/kg per hour or with an intravenous infusion alone at a rate of at least 0.14 U/kg per hour. Goal: decrease the serum glucose concentration by 50 to 70 mg/dL per hour or more. If the serum glucose does not fall by 50 to 70 mg/dL from the initial value in the 1st hour, the insulin infusion rate should be doubled every hour until a steady decline in serum glucose is achieved.

Insulin Therapy

When the serum glucose reaches 200 mg/dL ) in DKA or 250 to 300 mg/dL in HHS, the 09NSS is switched to dextrose in saline, and it may be possible to decrease the insulin infusion rate to 0.02 to 0.05 U/kg per hour. After resolution of DKA, pts treated with reg. insulin received subcutaneous NPH and regular insulin BID daily, whereas patients treated with IV glulisine insulin, receive glargine once daily and glulisine before meals.

DKA resolution

Normalization of the serum AG (less than 12 meq/L). Ketonemia and ketonuria may persist for more than 36 hours due to the slower removal of acetone, in part via the lungs. The patient is able to eat.

DKA resolution

IV insulin infusion can be tapered, and a multiple-dose subcutaneous (SC) insulin schedule started, in patients who meet the following goals:
Serum

glucose below 200 mg/dL. Serum anion gap <12 meq/L. Serum bicarbonate 18 meq/L Venous pH >7.30