acid base (hyperemesis/DKA)

7.35-7.45

pH normal values

35-45

CO2 normal values

22-26

HCO3 normal alues

accumulation of base

a. excessive use of bicarbonate

b. excessive use of antacids

c. lactate administration in dialysis

loss of acids

a. vomiting

b. nasogastric suctioning

c. hypokalemia

d. hypochloremia

e. administration of diuretics

f. increased levels of aldosterone

hyperemesis gravidarum

excessive vomiting 1st trimester peak 8-12 weeks usually resolves by 20 weeks

- increase in hCG, estrogen/progesterone

- potential cause: H-pylori

hyperemesis gravidarum risk factors

- genetic predisposition

- 1st pregnany

- multiple gestation

- previous pregnancy with HG

- pre pregnancy GU disorder

- pre pregnancy psychiatric diagnosis

hyperemesis gravidarum characteristics

- symptoms should start before week 16 gestation

- multiple times a day

- causing a change in food/fluid intake

hyperemesis gravidarum subjective data

a. mood - hx of anxiety, family hx of mental disorders, GAD questionnaire

b. hx of vomiting how long/frequency - any blood

c. fluid intake

hyperemesis gravidarum objective data

- tachycardia

- dry lips & mucous membranes

- weight loss

- orthostatic hypotension

- lethargy (later stage)

- hyporeflexia

hyperemesis gravidarum diagnostic tests

a. VBG (not ABG usually)

b. CBC

c. BMP/CMP

d. urinalysis

e. HcG

f. ultrasound

e. TSH/T4

urinalysis

this test would show ketones because after vomitting so much, they burnt fat and produce ketones

CBC

this test would should an elevated hematocrit due to dehydration and possible high WBC due to infection

hyper

someone with hyperemesis gravidum could get transient _______thyroidism

- hyper or hypo

PUQE-24

this test is used in pregnancy patients to assess N/V

- higher score = severe

HG maternal complications

1. Wernicke's encephalopathy

2. nutritional deficiencies

3. esophageal injury (tears)

4. coping: depression, anxiety

5. decreased maternal blood flow

6. preterm labor

wernicke encephalopathy

A disease of the brain that is the direct result of thiamine deficiency

- It causes confusion and makes people uncoordinated.

wernicke encephalopathy treatment

treatment:

IV thiamine infusion

- administration of glucose without thiamine can worsen this condition

thiamine

give ________ first before giving carbs

- what nutrient for Wernicke's encephalopathy

HG fetal complications

1. low birth weight

2. Intrauterine growth restriction (IUGR)

3. decreased placental perfusion

HG non pharm treatment

a. small meals multiple times a day

b. avoid spicy foods

c. avoid foods & stimuli that provoke symptoms

d. ginger gapsules/ginger mints

HG nursing management

1. thiamine pills

2. nausea pressure bands

3. acupuncture

4. G tube

5. TPN worst case

6. 5% dextrose

7. NS

8. antiemetics

antiemetic meds

- diclegis

- ondansetron

- metoclopramide

- clonidine

- promethazine (phenergan)

- prednisone

- mitrazapine

- dramamine

diclegis

antihistamine (H1 blocker) with vitamin B6 med used for N/V in pregnancy

- take at bed time because can make you drowsy/sleepy

zofran

avoid this antiemetic in first trimester if they can

- first line treatment in HG

DKA patho

insulin deficiency leads to hyperglycemia and triggers breakdown of fat cells resulting in increased ketones & glucose

DKA risk factors

a. a problem with insulin therapy - missed insulin doses

b. illness (increases insulin need)

c. other - chronic pancreatitis, alcohol, steroids, dehydration, post op, trauma, pregnancy

DKA clinical manifestations

- decreased LOC

- drowsy, confused

- fruity/acetone smelling

- kussmaul respirations

- N/V

- muscle weakness

- tachycardia

- arrhythmia risk

- polyuria, polydipsia, polyphagia

elevated

in DKA, glucose, potassium, and hematocrit will be ___________

- elevated or decreased

decreased

in DKA, chloride, pH, CO2, and HCO3 will be __________

- elevated or decreased

DKA lab diagnostics

1. ABG

2. CBC

3. BMP/CMP

4. urinalysis

5. anion gap

anion gap

normal 4-12

- check q6-8 hours

- we want to see it improving = the gap/# getting smaller

DKA potential complications

- dehydration/shock

- hypokalemia/hyper

- hypoglycemia

- MI

- stroke

- acute tubular necrosis (kidney injury)

- aspiration pneumonia

- cerebral edema

insulin

_________ will help treat the hyperglycemia, acidosis & hyperkalemia

250

add what blood sugar do we add in dextrose to continue insulin for DKA?

peaked T waves

elevated potassium can cause what EKG change?

MI

_____ and stroke are potential DKA complication due to the arrhythmia risk and viscous blood can cause a clot

cerebral edema

if glucose is lowered too quickly, rebound swelling of the brain can occur and cause further LOC decline

cerebral edema prevention

1. switch from 0.45% saline to NS

2. slow IV insulin rate

3. raise HOB

DKA initial treatment

- always start with NS

- tele

- IV insulin

- hourly CBG checks

- I&O

D5 1/2 NS

what hypotonic solution is sometimes used in DKA treatment?

true

true or false:

some form of IV dextrose (D5W, D5 1/2 NS, D50) is given in DKA in order to continue insulin till the anion gap is closed