MOD 5 RENAL AND ENDOCRINE ALTERATIONS

CHAPTERS 24-26, 30-32

Renal Assessment and Acute Kidney Injury (AKI)
 Key Assessment Tools:
• Laboratory Tests: Serum creatinine, blood urea nitrogen (BUN), electrolytes.
• Urine Output Monitoring: Critical indicator of renal function; assess for
oliguria or anuria.
• Imaging: Ultrasound to assess for obstruction; CT/MRI in specific cases.
 AKI Overview:
• Definition: Sudden decline in renal function, often reversible with prompt
intervention.
• Causes: Prerenal (e.g., hypovolemia), intrinsic (e.g., nephrotoxic drugs), and
postrenal (e.g., obstruction).
 Importance of Early Detection:
• Early identification and intervention can prevent progression to chronic
kidney disease (CKD) and reduce mortality.
Common Endocrine Emergencies
 Diabetic Ketoacidosis (DKA):
•Pathophysiology: Insulin deficiency leads to hyperglycemia, ketosis, and
metabolic acidosis.
•Key Signs and Symptoms: Polyuria, polydipsia, abdominal pain,
nausea/vomiting, Kussmaul respirations, fruity breath odor.
 Hyperosmolar Hyperglycemic State (HHS):
•Overview: Severe hyperglycemia without ketosis; typically presents in older
adults with type 2 diabetes.
•Symptoms: Extreme dehydration, altered mental status, seizures.
 Adrenal Crisis:
•Definition: Acute adrenal insufficiency leading tohypotension, electrolyte
imbalances, and shock.
•Triggers: Stress, infection, or abrupt cessation of corticosteroids.
•Recognition and Immediate Action:
 Rapid assessment and stabilization are critical to prevent life-threatening
complications.
Management of Diabetic Ketoacidosis (DKA)
 Immediate Interventions:
•Fluid Resuscitation: Restore intravascular volume with isotonic saline.
•Insulin Therapy: Continuous IV insulin infusion to reduce blood glucose and
suppress ketogenesis.
•Electrolyte Replacement: Monitor and replace potassium; anticipate shifts as
acidosis is corrected.
 Monitoring:
•Blood Glucose Levels: Hourly checks until stable.
 •Ketone Monitoring: Blood ketone levels to assess resolution of ketoacidosis.
•ABGs: Monitor pH, bicarbonate levels to gauge metabolic status.
 Goal: Correct metabolic derangements, restore normal glucose metabolism,
and prevent complications such as cerebral edema

Summary of Key Points

 Importance of Comprehensive Assessment:
•Use of laboratory tests, urine output monitoring, and imaging for
renal assessment; hormone levels and clinical presentation for
endocrine emergencies.
 Key Management Strategies:
o Tailored interventions for each condition: fluids, insulin,
electrolyte management for DKA; supportive care and hormone
replacement for adrenal crisis.
 Interdisciplinary Approach:
•Collaboration with endocrinologists, nephrologists, pharmacists, and
dietitians for holistic care.


Chapter 25: Kidney Clinical Assessment and Diagnostic Procedures
• Chapter 26: Kidney Disorders and Therapeutic Management
• Chapter 31: Endocrine Clinical Assessment and Diagnostic
Procedures
• Chapter 32: Endocrine Disorders and Therapeutic Management

Chapter 25: Kidney Clinical Assessment and Diagnostic Procedures

 Predisposing factors for AKI are obtained during hx and ick the use of otc meds, recent
infections, antihtn meds, and chronic use of NSAIDS can decr renal function
 FVE and edema are often seen in severe critical illness
PHYS EXAM:
Inspection:
 Bleeding:
o kidney trauma is suspected if purple discolouration is present on the
flank.
o Bruising, abd distension, and guarding are also signs of kidney trauma
 Volume:
o look for signs of FVD or FVE that may signal kidney issues.
o Assess JVD initially in supine position. ‘
o Also check CRT – if takes longer than 5 seconds indicates hypovolemia
o Skin turgor helps identify fluid related problems. If skin doesn’t retirn to
normal for several seconds – FVD – NOT APPLICABLE FOR ELDERLY
POPULATION
 Oral cavity can tell us if FVD is occurring but this can be affected by
o
meds used
 Edema:
o Sign of FVE
o May develop in the lungs or dep areas
of body
o Doesn’t always indicate FVE:
Hypoalbuminemia can cause third
spacing that results in edema, HF,
circulatory issues
o Pitting edema occurs when someone
places pressure over bony prominence and indentation doesn’t
disappear for 15+ seconds
Auscultation:
 Yields no useful info over kidneys
 Renal arteries can be auscultated for bruitis – can indicate stenosis
 Good for getting info related to extracellular FV status
 Heart:
o Assess R+R
o FVE is accompanied by extra heart sounds
o Incr HR + decr BP = hypovolemia
o Also assess for pericardial friction rub – indicates pericarditis and
uremia assoic w CKI
 BP:
o Good for determining FVD
o Orthostatic vital sign measurements indicate possible blood loss,
dehydration, syncope
 Occurs due to insufficient preload is available when pt changes
positions
 Lung assessment:
o Helps gauge fluid status – CRACKLE SINDICATE FVE
o Dyspnea with exertion, orthopnea,

Palpation
 Done by bimanual capturing approach
o Examiner shouldn’t be able to palpate L kidney but might be able to
palpate R kidney due to positioning
o Compare kidneys for size and shape and assess for irregularities

Percussion:
 Determine to detect pain in area of kidney
 Assess for air, or fluid accum around kidneys
 Also help determine size and location
  Doe by having pt lye on side – Costovertebral angle is struck – if rebound pain
= bad – infection or injury
ABDOMEN
 Observe and percuss abdomen
 Ascites is an important finding for FVE
 To determine if ascites for distortion done by producing fluid wave
ADDITIONAL ASSESSMENTS:
 Weight monitoring: sig fluctuation in BW over 1-2 days indicate fluid rather
than nutritional losses. Weigh pt regularly in CCU
 IN AND OUTS: helps eval fluid losses and gains more accurately. Kidney
disease causes psootive fluid balance leading to FVE, V/D/fever can cause
FVD
o Pts with CKI have oliguria – kidney function cannot be determined by
OUTS alone
o Gastric suction can cause abnormal OUTS snd cause severe A/B
balances
 Hemodynamic Monitoring
o CVD may be inserted to detect CVP (assess fluid vol status more
accurately
o Changes in CO and SVR can be seen in hypovolemic shock and can
elevate the MAP
 OTHER SHIT
o Kidney issues can cause electrolyte imbalances
 Less easily observable
o Pts with KF and incr in E- and nitrogenous waste products may exhibit
apathy, altered mentation
LAB ASSESSMENT:
BUN:
 Byprod of protein and amino acid metabolism
 Normal value is 5-20mg/dL = incr with CKD due to decr GFR and decr urea
prod
 Clinical signs = uremia symptoms
 BUn can be incr due to hypovolemia and other medications, hematoma
formation, excessive protein intake
 Decr in Bun = FVE, liver damage, severe malnutrition
Creatinine
 Brprod of normal cell metabolism – in serum and proportional to body mass
 Normal is 0.5-1.2mg/dL
 Higher in men than women – slightly
 Crea is filtered by glom
  Crea levels are not impacted by outside forces as much as BUN and thus are
a more sensitive and specific indicator of kidney function than BUN
 Impaired excretion results in high Crea in pts with kidney failure
 Malnutrition, muscle wasting disorders can alter Crea levels
BUN-CREA RATIO
 Usual ratio is 10;1 – changes to this may indicate renal dysfunction
 Better indicator of prerenal kidney failure than separate tests alone

Crea Clearence
 Urine crea clearance tells us how good to kidneys are at filtering out
creatinine
 Ability of kidneys to clear crea from blood is indicator of how well the
glomeruli and tubules are working
 Normal value is 110-120mL/Min
 Anything lower indicates renal dysfunction
 Measured via 12-24 hour urine and blood sample collection
Cystatin C
 Not widely used
 Cystatin C are usually very low bc the glom filters them out of body – in KD,
glom filtration of CC is reduced and not given to tubules for metabolism
Osmolality:
 Reflects the conc of dilution of vasc fluid
 Normal values 275-296 mOsm/L
 Elevated value = dehydration
 Decr value = FVE
 If serum osmolality incr = ADH incr = water reab from kidneys = return to
serum osmolality
 Opposite occurs with FVE
 Measured serum osmolality is useful in determining fluid balance and fluid
replacement therapy for CCU pts
 Decr serum os may indicate ADH disorders
Ion Gap
 calc of the diff btwn the measurable extracell plasma (Na + K+) and the
measurable anions (Cl- and Bicarb)
 in plasma = Na is predom cation and Cl the predom anion
 normal anion gap is 8-16 mEq/L
 acute and CKD can incr the anion gap due to retention of acids and altered
bicarb resorption.
Hgb and Hct
  indicate incr or decr in intravasc fluid volume
 values vary btwn sexes
 Men: 13.5-17.5g/dL HCT: 40-54%
 Women: 12-16g/dL, HCT: 37-47%
 HCT: value is the proportion/conc of RBCs in volume of whole blood and is
shown as a percentage
 Incr in HCT = FVD = hemo conc
 Decr = FVE = via fluid loss, blood loss, liver damage
 IF HCT VAL IS DECR BUT HGB REMAINS CONSTANT = CAUSE IS FVE
Albumin
 50% of total plasma protein is serum albumin
 Normal value is 3.5-5 g/dL
 Res for the maintenance of colloid osmotic pressure – holds fluid in vasc
space
 In some diseases albumin is lost form vasc space = third spacing = edema
 Elevated albumin levels are rare
URINALYSIS:
 In critically ill pt = routine UA are done to r/o presence of urinary protein or
glucose
 Urine appearance: urine colour, clarity, odour – colour can be impacted by
medication or food, clarity- bacteria or wbc, odour – conc or infection
 Urine pH: determine alkaline or acidic urine – ranges btwn 4.5-8. Change sin
metabolic function and kidney function prod changes in urinary pH
o Ince acidity = retention of Na an acids – intrarenal KD
o Basic urine is due to body retaining bicarb
 USG: measures the density or weight f urine in comp to distilled water
o USG should always be higher than water
o Normal values 1.005-1.025
o Reflects hydration status and tells us if kidneys can conc or dilute
urine
o Dcer in USG reflect inability of kidneys to conc urine
o Incr in USG = dehydration, protein, or glucose that incr urine density
 Urine osmolality:
o Normal values are 500-1200 mOsm/kg and depends on resorption or
excretion of water from kidneys
o Incr in osmolality accompanied by decr UO during FVD is due to
retention of bodily fluids
o Decr in osmolality accompanied by incr UO during FVE bc fluid is being
excreted from the kidneys
 Urien Protein:
o Should be relatively absent form urine
o Values higher than 150mg/day signal glom compromise and intrinsic
KD
o Both the amount of protein and crea are measured in urine
  UPC normal value is <0.2
 UPC higher than 3.5 indictas that 3.5g are being excreted by
kidneys per day = sig KD
 Urine glucose
o Urine should be free of glucose
o shouldn’t exceed 130mg/day
o in CCU only serum gluc is measured as glucosuria is not good indicator
bc of damaged nephrons
 ketonuria
o shouldn’t be present = if present = hyperglycemia caused by T1D or
starvation ketosis
 Urine electrolytes
o Urine Na: most common measured E- in urine and reflects aldosterone
and subsequent retention and excretion of Na by kidneys to maintain
fluid balance
 Hypovolemia = Na urine is low
 FVE = Na urine is high
 Amount of Na in urine can help determine pathology of AKI if
diuretics haven been given
 Urine sediment:
o Epithial cells and casts in urine aid to identify problems r/t to kidneys
o Fresh urine sample is important – 30-60 minutes old
o Presence of absence of sediment is good at identifying cause of AKI –
prerenal, renal, or post renal
 Prerenal =no sediment
 Intrarenal – glom are damaged – casts and sediment in urine
o Casts: cylindrical structures composed of mucoprotein which is
secreted by LOH, distal tubules, and CD
o Casts differ in comp and size and corelate to the severity and type of
KD
 Wbc casts indicate pyelonephritis
 Rbc casts indicate glomulonephritis
 Hyaline casts indicate kidney parenchymal disease and glom
cap membrane inflammation
 Epith cells that are constantly in urine indicate nephritis
o Hematuria:
 Both obvious and occult hematuria may indicate KD
 Micro can occur after strenuous exercise or catheter
insertion
 Myoglobin can make urine appear red – may result from
MSK damage \
 Rhabdomyolysis can develop in CCU pts for multiple
reasons – injury, status epilepticus,
URIEN TOX SCREEN
  Can be screened to detect alcohol, illegal drugs, nonprescription meds, etc –
any sub excreted by kidneys
 Urine tox screens taken in CCU are screening tests and are not dx of a
disease state
 Used to detect reasons for altered mentation or LOC
IMAGING STUDIES:
 Imaging studies can determine can confirm or clarify causes of particular
disorders
 u/s non-invasive technique helps determine size and shape of kidney and
contours, look for cysts and masses
 some contrast agents are nephrotoxic – cant be given to everyone
o pts with high risk incl having preexisting kidney injury, have crea
clearence above 1.5mg/dL, older than 75, taking meds such as
antidiuretics, ACEI, ARBs.
o ADEQUATE HYDRATION IS ESSENTIAL FOR CONTARST STUDIES TO
AVOID THE RISK OF CONSTRAST INDUCED NEPROTOXICITY
 KIDNEY BIOPSY
o Incr US has lead to incr dx of tumors
 Biopsy is needed to dx disease processes involving the kidney
parenchyma
 BIOPSY IS LAST CHOICE FOR DX ASSESSMENT IN CRITICALLY ILL
PTS DUE TO PROCEDURAL RISKS OF BLEEDING, HEMATOMA,
AND INFECTION
+++++++++ +++
+++++++++ +++
+++

CHAPTER 26
KIDNEY
DISORDSER AND
THERAPUTIC
MANAGEMENT
AKI:
 Spectrum of
acute onset
kidney
disorders that
can range form
mild to acute
kidney failure
and aids

intervention evalualtion
 AKI Described as sudden incr in crea and abrupt decr in UO indicating dcer
GFR and retention of byproducts in blood
 AKI disrupts acid-base homeostasis, FV equim, and E- balance
CRITICAL ILLNESS AND AKI
 Pts with AKI in ICU have longer hosp stays and higher mortality rates – 10-
50%
 Poir survival rates is usually due to coexisting conditions that incr sus to AKI –
 Most common causes of AKI are sepsis, hypovolemia, drugs, and cardiogenic
shock

DEFINITIONS OF AKI
  Wide variations of descriptions
 Measurement of kindey function is indirect dx of AKI is due to change sion UO
and incr serum crea – these detect changes in GFR
 UO not great as it can be altered by diuretics
 RIFLE CRITERIA
o Risk, Injury, Failure, Loss, and End stage
renal disease
 AKI into 3 categories (RIF)and 2
outcome criteria (LE) based on
GFR status reflected by change in
UO or loss of kidney function

AKI Network Criteria:

 Like RIFLE.
 Both indicated in a critically ill pt changes in
serum crea and uO may signal declines in
kidney function
 Severity if injury is described from 1-3 – using
serum crea, UO, use of renal replacement therapy and eGFR

675
Types of AKI
 Prev defined by location of insult, (pre=intra-post renal) – not really used nay
more
 Prerenal:
o Any issues that decr Bf, BP, or kkindey perfusion before arterial blood
reaches the renal artery
o Due to hemorrhage, vasodilation, or thrombus – ANYTHING THAT
CAUSES DECR BF TO KIDNEY – GFR DECR AND UO DECR
o WHY NURSE SIN CCU MONITOR UO SO CLOSELY
o If perfusion is re-estab early on – little to no perm damage occurs
o Pt can develop oliguria if not treated promptly
o Prerenal azotemia is associated with lower mort rate than other forms
of AKI
 Intrarenal AKI
o Anhy condition that causes ischemic or toxic insult to parenchymal
nephron
o Can be caused by prolonged hypotension or low CO
  Meds induced damage incl abx and contrast dye used for
urology studies
 Postrenal AKI:
o Anything that prevents the flow of urine
o Uncommon cause of AKI in CCU pts
o Sudden development of anuria should prompt verification that UO is
not occluded

\
\
ASSESSMENT AND DX
 Lab assessments
o Serum E-:
 E- in serum become extremely elevated when AKI is present
o Urine E-
 Also altered by AKI but don’t help with predicting outcome of
illness
 RARELY MEASURED
 o PRE VS INTRA- RENAL
 BOTH SERUM AND URINE E- can be used to assess whether AKI
si at a prerenal stage
Acidosis
 pH <7.5 is sign of severe kidney insult
 metabolic acidosis occurs due to metabolite build up and decr serum ph
 resp and mech vent aren’t enough to cure this
 acidosis secondary to AKI is very complex as many pts have norma anion
gap+
BUN
 Unreliable indicator of kidney injury as indiv test
 Bun changed by protein intake and blood in Gi Tandc an be diluted with fluid
admin
 BUN-CREA ratio is most useful in dx AKI where Bun is very high relative to
serum crea and pts can be developing AKI before becoming symptomatic
 Azotemia
o Incr in Bun level – assoic with AKI
o Uremia is another way to say elevated BUN levels
 Serum crea:
 Byprod of muscle metabolism
 Crea is completely excreted in healthy kidneys
 When Aki present kidneys no excrete
 Even low incr in serum crea can repress sig decline in GFR
 Crea clearence: normal rate is 120mL/min but this decr with AKI
o CC pts pay show signs of olguria
o MEASURED IN CRITICAL ILLNESS
 Fractional excretion fo Na
 FENa can be measured in urine early in the course of AKI
to diff btwn prerenal and intrarenal AKI
 FENa value <1% = prerenal compromise = bc resorption
of all filtered Na is appropriate comp mech when decr
kidney perfusion
 FENa value over 2% = kidney cannot conc Na
 RARELY USED
AT RISK DISEASE STATES AND AKI
CKD:
 Practice guideline management endstage renal failure into 5 stages
Cardiorenal syndrome
 Strong assoic with CKD and HF
 5 types under term cardiorenal syndrome (CRS)
1. Type 1 CRS: acute HF that causes AKI
 2.T2CRS: chronic HF that results in AKI
3.T3CRS: AKI causes acute HF
4.T4CRS: CKD that causes chronic HF
5.T5CRS: a systemic condition that damages both he heart and
kidney
 Maintenance of BP under 130.80 and BG WNL decr risk of developsing CKD
and CVD
RESP FAILURE AND AKI
 Sig association btwn the two
 PEEP vent reduces BF to kidneys and lowers GFR and UO
 Management rec are lung protective vent, conservative fluid management,
and early recog + trmt of pulm infections

SEPSIS AND AKI

 Causes almost 1/2 of cases of AI in CCU Pts
 Create hemodynamic instability that reduces BF to kidneys
 Vasopressors can incr bp and SVR but they may incr resistance in kidney
microvasculature
TRAUMA AND AKI
 Traumatically injured pts have different demographic profile than other AKI
injuries – due to trauma mainly in younger males with no preexisting
condition
o Rhabodomylosis:
 Occurs with major crush injuries and incr risk of RF due to
release of crea and myoglobin
 Focus on serum potassium as life threatening levels can occur in
pts with this as cell lysis releases potassium into serum
 Crea kinase is a marker to detects systemic muscle damage
 Crystalloid vol resus is the primary trmt for this
 Close monitoring of pts hourly UO, CK levels, serum crea levels,
serum potassium levels and signs of compartment syndrome
Contrast induced nephrotoxic and AK Injury
 Pts at highest risk are pts with preexisting kidney issues, elevated crea, and
dehydration
 Radiopaque contrast medium: nephrotoxic: highest risk pts are those with
preexisiting kidney failure and a low eGFR are at highest risk
o Promote hydration and avoid dehydration: aggressive hydration with IV
saline during + after procedure ‘
 Medications: Nephrotoxic meds are stopped prior to procedure
 Mainstay measures are to use lowest contrast needed, stop all nephrotoxic
meds, provide aggressive fluid resus, ad avoid repeat contrast injections
within 48 hours
CAUTIs
 Many critical ill pts have indwelling UCATH to record UO accurately
 CI Pts are at highest risk for developing a CAUTI and subsequent UTI
o Avoid unnessessary use of catheters
o Use aseptic technique when inserting ucaths
o Adopt evidence based standards for UCATH maintenance
o Review the need for indwelling UCATH daily
o Remove catheter ASAP

HEMODYNAMIC MONITORING AND FLUID BALANCE

 Monitor for changes in vitals and CO
 Daily weight – weight gain over 1kg in 24 hours repress sig fluid retention –
need to have accurate INS and OUTS to do this best
 Phys assessment:
o Fluid depletion: decr skin turgor, lethargy
o FVE: pulm congestion, incr HF, and incr BP
o Pt with untreated AKI is edematous: fluid retention, low serum albumin
levels, inflam assoic with AKI
 o Assess freq for pitting edema over bony prominences and in dep body
areas
 E- Balance
o Potassium: hyperkalemia is a risk for all phases of AKI. Severe
arrhythmias can result : peaked T wave, wide QRS, VTACH and VFIB
 Acute hyperkalemia can be reduced insulin and dextrose
 In nonemerge settings beta 2 agonists ad loop diuretics can
reduced high k+
o Sodium: both hypo and hyper natremia are assoic with incr mortality
with KF
o Ca and P: Ca levels are reduced in KF. High P levels are associated with
greater mortality rates as well
 High P causes low Ca – pts should take oral phosphate binders
 CA REPLACEMNT
 Can be measured by total Ca or ionized Ca
 Total Ca not really accurate
 IONIZED CA: (metabolically active, nonprotein bound) is
preferred measurement
 Take Ca supplements to prev hypocalcaemia
MEDICAL MANAGEMENT OF AKI
Treatment goals: prev, comp for KI, and regen of kidney function: fluid balance,
anemia, meds, and E imbalance
 Prevention
o Best method/remedy for AKI
o Assess pts risk for AKI
o BSAIDS should be avoided in ots with elevated creatinine
o Use contrast as last resort

Fluid ressuscitation
 Prerenal AKI si cause by decr perfusion and flow to the kidneys
 Objectives for fluid resus are to replace fluid and prevent further loss
 Adults req 1500mL/m2 oer 24 hours
 Other important criteria to consider is baseline metabolism, fever, temp, and
humidity
 Crystalloid and colloids
o Freq monitoring of serum E is crucial and strict I+Os are used
o Crystalloids:
 Widespread use for IV maintain infusion and replacement
therapy
 Lower mort rates with this IVF
o Colloids:
 Contain oncotically active particles that expand intravasc
volume and achieve hemodynamic stability
 Albumin main colloid used
  Colloids can last 24 hours
o Little difference in the 2 IVF in CC Pts with AKI
o Fluid resus in pts with AKI:
 Fluid restriction is a mainstay of med management: prevents
FVE and circ overload
 Daily weights and accurate I&Os is essential for fluid
management
 Pts with KF are restricted to 1L of fluid/24 hours if UO 500mL or
less
o Fluid removal: AKF results in retention fo water,toxins and solutes in
the serum
o Diuretics to stim urination are use din early AKI
o Hemodialysis is another choice if FVE worsens pulm edema, or HF

PHARMACOLOGICAL MANAGEMENT IN AKI

 FIRST STEP IS TO STOP ALL NEPHROTOXIC MEDICATIONS
 Decr freq of admin or decr dose and monitor concentration by measuring
serum med levels
 Diuretics: stim UO in ots with FVE with working kidneys
o Prevtn E- imbalances as this can happen with too high doses of
diuretics
o Good for issues such as pulm edema BUT DON’T PREVENT AKI
o Loop diuretics:
 Furosemide most commonly used in CCU – E= abnormalities are
common must closely monitor for serum K+, Na+ and Mg+
o Thiazide duietics:
 May be given following a loop diuretic as they act on different
parts of the nephron
 Crea clearance effects efficacy of thiazide
o Osmotic diuretics:
 Mannitol
 To incr UO and decr FVE
 Filtered by glom and isn’t absorbed by nephron and works in
proximal tubule and DLOH
o Carbonic anhydrase inhibitor diuretics
 Used in very specific circumstances
 Treats metabolic acidosis that occurs with loop diuretics
o K+ sparing diuretics:
 Inhibits aldosterone in distal tubule causing K+ to be retained
 Vaptans:
o Newer class of med inhibit ADH in aquaporin channels
o Helps correct symptomatic hypervolemic hyponatremic states
o Cannot be sued for hypovolemic hyponatremic states or anuria
 Dopamine:
o Helps stimulate BF to kidneys
 o Helps incr UO short term
o Doesn’t prevent AKI
 Dietary P+ binders
o Many available
o Have to be take with meals
o Depends on quantity of Phosphorus in diet

Nutrition:
 Rec energy intake is 20-30kcal/kg per day with 1.2-1.5 g/kg of protein to
control azotemia
 Oral nutrition is preferred
 Fluids limited, BP measured and BG measured recommended
 E- Na Kand P are strictly limited
NURSING MANAGEMENT OF AKI
Prevention, level of kidney function, risk of infection, fluid imbalance, E
disturbances, anemia, UCATH care
Risk factors for AKI
 Pts include d=elderly pts, dehydrated pts, and pts undergoing contrast dye
studies
CAUTI MANAGEMENT
 Signs of UCATH infection incl fever incr WBC, or redness around wound or
catheter site
 Remove catheter ASAP – if pt cannot pee several methods can be used other
that reinsertion: bladder scanner, intermittent catheterization are both
methods to use before indwelling UCATH
FLUID BALANCE
 Intravasc volume assessed on hourly basis for CI pt
 Hemodynamic values, and daily weights are corelated with I&Os
 UO is measured hourly by UCATH and drainage bag through all phases of AKI
particularly in response to diuretics
 Need to be vigilant of signs of FVE: dep edema, ascites, pulm edema, heart
sounds, and brain ICP
E imbalance
 High K+ & P+ and low Na+ and Ca+ occur in AKI along with acid-base
imbalances
 Clinical siugns must be avoided and their side effects controlled
 High P can cause pruritic
Prevent anemia:
 Expected side effect of KD due to lack of EPO production
  Prevent blood loss in pt with AKI and reduce need for blood WD
 Irritation of Git due to metabolic waste build up is expected
 Give EPO stim meds along with iron, vit b12 and b6’
EDUCATE FAMILY
 Prognosis, trmt, complications
 Sleep rest disorders can occur
 Encourage family to voice concerns frustrations and fears
RENAL REPLACMEENT THERAPY
 Two kinds to treat AKI: intermittent hemodialysis and cont renal replacement
therapy (IHD & CRRT)
 Hemodialysis separates and removes excess electrolyse, fluid and toxins form
he blood via a hemodialyzer
o Artificial kidney:
o A dialysis nurse or technician
inserts two needles into the
patient's arm.
o The needles are attached to soft
tubes that connect to the dialysis
machine.
o The patient's blood is pumped
through the dialyzer, which is
located outside the body.
o The dialyzer filters the blood,
removing waste, excess fluids,
and salts.
o The cleaned blood is returned to
the patient's bod
o Trad hemodia lasts 3-4 hours

Vascular access
 Hemodialysis req vasc access
 Temp vasc access:
o Subclav and femoral veins
o Duel lumen catheter most commonly used : helps prevent
dialyzing same blood that’s was just returned to area
 Perm vasc access
o AVF: sx exposing peripheral artery and vein – creating side by
side opening in the artery and vein and joing the two together
 Preferred method of access bc the durability of the BV, few
complciations, and less need for revision compared to
other methods
 Need to wait 14 days after sx revision to start dialysis –
temp dialysis is needed
 Ideally fistula is created 6m prior the need for
dialysis
 Nurse must assess for quality of BF through the fistula
 Patent fistula will have a thrill when palpated gently
 NO BP MEASUREMNTS, IV INFUSIONS OR
PHELBOTOMY ARE TO BE DONE ON FISTULA ARM
o AV Grafts
 Connect vein to artery via graft
 2 Large bore needles are used for inflow and outflow to the
graft during dialysis
o Tunnelled catheters
 While waiting for fistula or graft some pts have tunneled
catheter placed in jug vein
MEDICAL MANAGEMENT\
 Decision to place device and to choose the most appropriate type and
location for each patient
 In CUU: use temp hemodialysis catheter
Nursing management:
 Non CCN trained in dialysis manages the IHD
 In ccu hemodialysis occurs daily
 Roe of CCN is to monitor pts hemodynamic status and ensure they
remain hemodynamically stable
CRRT:
 Cont mode of dialysis that’s been used for 40+ years
 May cont over many days
 The crrt system allows for cont removal of fluid form plasma and
dialysis rate is ~20-30mL/kg per min
 Fluid removal rate dep on patient
 Hemodynamic stability can be maintained via this machine – BIG PRO
for use on hemodynamically unstable patients with many issues
 Modes of CRT
o CVVHD: Primarily removes waste products through diffusion,
where solutes
o SCUF: Focuses primarily on fluid removal with minimal solute
clearance
 o CVVHDF: Combines both convection and diffusion for a more
balanced solute removal
o CVVHD: Primarily removes waste products through diffusion,
where solutes move across a concentration gradient from the
blood to the dialysate
MEDICAL MANAGEMENT
 No best choice for blood purification to treat AKI
 New method is to start either IHD or CRRT sooner than later to prevent
serve AKI issues for pts who are hemodynamically unstable
o Threshold to begin pt trmt depends on many factors: serum
creatine, FVE, E- imbalance
o Another issue is when do we stop this therapy? Or how do we
determine when kidneys have recovered enough – one rec is UO
of 500mL/day
NURSING MAAGEMENT
CC nurse monitors fluid intake and output, detect issues, identify E- trends,
supervises safe CRRT use and provides pt and family education about pts
condition and use of crrt

PERITONEAL DIALYSIS:
Less high tech modality used for CKD
Peritoneal dialysis (PD) is a treatment for kidney failure that uses the lining of the
abdomen to filter blood. It's a home-based treatment that involves filling the
abdomen with a cleansing fluid, called dialysate, to remove waste and excess fluid.
How it works
1. A surgeon places a catheter into the abdomen.
2. Dialysate is delivered through the catheter into the abdomen.
3. The dialysate absorbs waste and extra fluid from the blood vessels in the
abdomen.
4. The dialysate is drained and replaced with fresh fluid
Infection is highest risk to pt with the use of PD is peritonitis and sepsis
Nurse smust be vigilant to detct digns of localized catheter or abd infection, monitor
fluid volume status, infuse the dialysate and observe drainage and provide pt and
fam education
CHAPTER 31 764
Endocrine Clinical assessment and DX procedures
Endocrine assessment focuses on
1. Current health status
2. Description of current illness
3. Med hx
4. Fam hx
PANCREAS
 Insulin is made by the pancreas
 Abnormal gluc metabolism incl hyperglycemia – maybe prediabetic, or due to
sevre illness or t1d or t2d
 Hyperglycemia
o Affects all parts of the body
o S+s incl blurred vision, headache, weakness, drowsiness, a/n/v
o Inspection: flushed skin, PU/PD, V+, dehydration
o Dcer lo cis seen with sevre elevations in hyperglycemia
o Ketoacidosis can occur – kusmaul respirations can occur with a fruity
odour to the breath
o Asuc of abd may incl hypoactive bowels
o Palp elicits abd tenderness
o Percussion: decr dtr
o Signs of dehydration incl: tachycardia ohtn, and poor skin turgor

Lab studies:
 Test for pancreatic function and LT BG levels
BG:
  Fasting plasma glucose is done by blood test after pt not eaten for 8 hrs
o Normal value is 70-100mg/dL
o Prediabetes 100-125mg/dL
o 7mmol/L = diabetes
 Normal postprandial BG levels should be <10mmol/L
 All critically ill pts need their BG checked regularly
 Institute insulin therapy when BG is > 180mg/dL
 Target BG 140-180 is rec
 During insulin therapy -bg is tested reg to ensure its not dropping too much

URIEN GLUCOSE
 Not rec for pt with diabetes bc fluctuations exist depending on the extent of
kidney damage
 Uren also cant detect hypoglycemia
 NEVER USE THIS
GLYCOLATED HEMOGLOBIN
 BG testing of glucose is useful for daily management of diabetes
 Glycolated hbg tells use the average BG of a pt over =3months
  A1C less than 7% is the target for a pt with diabetes
 No diabetes A1C <5.7%
 PREDIABETES = 5.7-6.4%
 DIABETES >7%
Blood ketones:
 Byprod of rapid fat breakdown
 They rise I acute illness, sevre t1d,
 Ketone breath smells fruity
 Pts should have their blood tested for ketones if altered LOC, acute illness or
iccr BG level– urine test not reliable

PITUITARY GLAND
 Cant phys assess it
 Nurses must be aware of systemic affects of normal functioning vs abnormal
 ADH/VASOPRESSIN is released from this gland
 Secreted during hypovolemia, change sin serum osmolality, hypoxia, and
acidosis
 ADH actions are both antidiuretic and vasoconstriction
PHYS ASSESSMENT
 ADH controls fluid retention in the body
 Injury to hypothalamus may cause altered ADH secretion
 Clinical signs of pituitary dysfunction are: FVE or FVD
 Hydration status
o Hydration assessment great to determine ADH function
 Should assess skin turgor and buccal membrane moisture
 Skin turgor test that returns immediately = adequate hydration
 Can also assess mentation, USG, edema, daily weights
 Vital signs
o Changes in HR, BP, and CVP are good at determining fluid balance
 Decr BP and Incr HR = FVD
 Incr HR and BP, and bounding pulse = FVE
 Weight changes and I&Os
o Daily weight changes coincide with fluid retention or fluid loss
o To determine fluid loss or retention besy – extraneous values must be
eliminated
 Use same scale, weight at same time of day, precises I&Os are
recorded
LAB ASSESSMENT
 No single test can be dx of pituitary dysfunction : Made mainly through
clinical pres and pt hx
 Serum ADH
 o Normal ramges is 1-5pg/ml
o Meds that may alter ADH prod are stopped for 8 hours before test
o This value is compared with blood and urine osmolality to diff btwn
SIADH and DI
 Serum and urine osmolality:
o SERUM Ranges form 275-205 mOsm/kg H20
o Determine conc of dissolved particles in a solution
o In healthy ppl change in solute conc trigger comp mech to maintain
serum level
o Incr serum osmolality stims ADH release and incr fluid volume in blood
o Decr serum osmolality decr fluid in serum
o Urine osmolality has a wide range of 50-1400 mOsm/kg as it fluctuates
with fluid intake
 ADH test
o Diffs btwn centrl DI or kidney DI
o Urine vol and osmolality are tested q30min FOR 2 HRS
o Nephrogenic kidneys don’t res to exogenous ADH and urine osmolality
remains unchanged
o These tests are done on CCU as they can worsen hemodynamic
instability and volume status
 Copeptin:
o Copeptin is a biomarker released with ADH
o Good test as it reliably relate to ADH levels in both healthy and
critically ill pts
o More stable in blood allowing for reliable measurement
o Useful for diff btwn nephrogenic DI and partial central DI

Diagnostic Procedures
 Xrays, Ct and MRI can help detect brain abnormalities – csnt dx DI and SIADH
BUT CAN HELP TERMINE UNDERLYING CAUSE
o XRAYS – can determine fracturs or swelling at base of brain and
suggest interference with blood supply to areas of the brain
o CT – identifies tumours, blood clots, and tissue masses. Size , shape
and location fo hypothalamus and pituitary can also be identified
o MRI: visualize in ternal organs and cellular chars of tissues. Soft brain
tissue amd surrounding CSF make brain suited for assessment with MRI
THYROID GLAND:
 CLINICAL ASSESSMENT
o HX: detailed as possible – identify s+s of hypo or hyperthyroidism
o PE: thyroid palp for tenderness, nodules, enlargement and bruits
o Normal thyroid isn’t seen nor is it palpable
o Bruits indicate enlarged thyroid and icnr BF to glandular tissue
 LAB STUDIES
o controversy exists about routine thyroid monitoring
 o TESTING IS REC FOR PTS 60+
o No rec screening fir CCU pts
o Measure levesl of circ thyroid hormone and asses in the of neg
feedback response of the hypo-pit-thyroid axis
o Thyroid blood test measures TSH and free thyroxine 4: TSH is inhib but
FT4 in blood and tsh levels are normal
 Inverse linear relat btwn 2 hormones exist
 Hypothyroidism: high TSH low FT4
 Hypothyroidism: low TSH and High FT4, and incr FT3-FT4 ratio
o TSH SCRENING
 TSH is more sensitive for low TSH lebesl
 Serum TSH incr as pt grows older
 TSH 0.4-4.3 milliunits/L between 20-59 yoa
 TSH 0.4-5.8 milliunits/L between 60-79 yoa
 TSH 0.4-6.9 milliunits/L for 80+ pts

 Thyroid test in critically ill pts

 Incidence of thyroid issues low in CCU
 When present in CCU – TSH measurement is first test
doen but experts rec TSH and FT4 should be taken
o MEDS AND THYROID TESTING
 Tsh is affected by many eds given in CCU – dopamine block TSH,
amiodarone is struct similar to T3 and T4
 Meds that in FT4 – incr ft4 by displacing protein bound T4
 ASA, Lasix, and UF and LMWH raise FT4 bu this mech
 Unclear if ppl in CCU should adjust to pharm measures in
Ci pts
o DX procedures
 US to visualize tumour
 Oral radioactive isotope o detect hyperthyroidism
ADRENAL GLAND
 Primary adrenal disorders
o Primary indicates issues lies in adrenal gland
o Secondary is due to other organ system
o Adrenal cortex secretes 2 hormones and abnormalities can lead to
clinical s+s
 Releases cortisol and aldosterone
 Cortial is released in res to stress
 Aldosterone is released in res to intravasc hypovolemia
o Adrenal medulla secretes epinephrine and norepinephrine
 Both hormones excretes in res to stress
 CLINICAL ASSESSMENT
o HX: can help identify issues with adrenal glas
  Primary endocrine disorders are rare but uncontrolled HTN
should be investigated
 Steroid use should also be investigated – cream, inhalers
 PHYS ASSESSMENT
o Methodological approach to assessing S+s is essential as adrenal
issues are often missed or misdiagnosed
 Adrenal cortex
o Primary cushing syndrome: caused by excess cortisol secretion
 Rare – dr must r/o other conditions
 First step is to get ACTH stim test - serum level <2.2pmoL is
considered dx
o Secondary cushings syndrome
 Symptoms are same as primary
 Pts may be taking glucocorticoids for chronic inflam disorders
and after organ transplant

Primary Aldosteronism:
 In primary aldosteronism adrenal cortex secretes aldosterone unrelated to
RAAS
 Severe untreatable HTN and hypokalemia can result in ER
 Dx test for high risk individuals is aldost to renin ratio
 Ct scan may be done to detect tumours
Adrenal insufficiency
 Hyposecretion of cortisol and sometimes aldosterone
 ADDISIONS DISEASE: seen as inverse s+s of Cushing’s
 Dx tets involves simultaneously testing for ACTH along with cortisol serum
levels
 Low serum cortisol with incr ACTHA OR serum cortisol below 100nmol/l in AM
is considered DX
ADRENAL CRISSI AKA ADDISONIAN CRISIS
 Life threatening condition where adrenal gland is almost nonfunctional
 Pt presents with critical hypotension, hyperkalemia, hyponatremia, and
hypoglycemia
ADRENAL MEDULLA:
 Pheochromocytoma: rare tumours that arise catecholamine producing
chromaffin cells of adrenal medulla and excrete excess norepi and epi in high
amounts
o When this happens a catecholamine storm happens
o Dx test are to measurement of plasma and urine unfractionated
metanephrines
o CT is sued to asses adrenal glands
CHAPTER 32 ENDOCRINE DISORDERS AND THERAPUTIC MANAGEMENT
ACUTE NEUROENDICRINE REPOSNE TO CRITICAL ILLNESS
 Major neuroendocrine disorders occur wen phys stress caused by critical
illness, CVD, sepsis, trauma occur
 HPA axis is exaterbated in critical illness
 Fight or flight is rapid discharge of catecholamines noreoi and epi
HPA axis in critical illness
 Pit gland has two parts
o Posterior pit produces ADH – COMP OF STRESS RESPONSE
 When combined with epinephrine – BP raises quickly
o ANteror ot gland produces corticotrophin – stims cortisol release
 Also stims hyperglycemia that is seen in critical illness
 Adrenal gland produces cortisol contributing to the stress responses
 In res to critical illess – we see an initial high cortisol level
 BUT IF STRESS RES IS SUSTAINED: CIRCI can occur
HYPERGLYCEMIA IN CRITICAL ILLNESS:
 Many factors incr glucose: glucagon, cortisol and epinephrine
 Glucagon is released in res to stress by pancreas
o Normal feedback loop that controls glucagon release is disrupted in
critical illness or diabetes
o Glucagon can be incr 5x unrekated to insulin in CI which causes
hyperglycemia
o This also stims release of cortisol and epinephrine and further stim
glucagon release in the liver
o Insulin release is decreased in acute CI
o Insulin indep GLUTs are active during stress (helps secrete insulin) but
may become overwhelmed with massive incr in gluc prod
o Managing glucagon release in CCU is not feasible
o Hyperglycemia management focuses on cont infusion of insulin to
maintain BG levels within acceptable ranges
HYPERGLYCEMIA MANAGEMENT IN CRITICAL ILLNESS
 Normal fasting BG levels are 70-100mg/dl
 CI pts have higher BG levels and are at an increased risk for mortality
CLINICAL PRACTICE GUIDLEINES FOR BG CONTROL IN CI PTS
 Rec use of insulin infusion to maintain BG in CC Pts between 140-180mg/dl.
This range was selecte to minimize risk of hypoglycemia and prevent extreme
hyperglycemis
 Insulin management must occur if BG >180mg/dl
INSULIN MANAGEMENT IN CI PTS
  Freq BG monitoring
o If bg >180mg/dl pt is started on cont insulin infusion
o After ot is stable Bg tests can be spaced from q1hr to q2hr
o Several diff Bg sampling methods are available
 Finger prick – fingers can get trauma if too many Bg samples are
takend
 Central venous catheter is in – highly efficient Bg sampling
 Point of care testing for BG in CI
o Handheld glucometer is freq used to allow hourly rapid assessment of
BG and titration of cont glucose infusion
Continuous insulin infusion
o Insulin infusion protocols for management of stress induced hyperglycemia
have been set up in hospital
o Effective BG protocols Gauge the insulin infusion rate based on 2 parameters
o Immediate BG result
o Rate of change in the BG level since last measurement
o MOST IMPORTANT PAINT TO EMPHASIZE THE RATE OF CHANGE OF BG
IS AS IMPORTANT AS LAST BG LEVEL
o Fluctuations in res to changes occur and alter BG such as stopping
enteral or parenteral nutrition, admin of therapeutic steroids, bc the
person is less catabolic
o Incorp bolus insulin doses if BG >180mg/dl

TRANSTION FROM CONT INSULIN INFUSION TO SQ INSULIN

 Must be handled with care to avoid large fluctuations in BG levels
 Infusion should be at a stable and low rate
 Transition dep on many factors incl if pt can eat enough
 Drs use many methods to calc quality o insulin to prescribe during transition
from IV to SQ insulin to maintain stable BG levels
 Many types of insulin are available for use
 After transiotn – Bg needs to be monitored freq to maintain BG in constant
range and detect hypo or hyper glycemia
 Corrective insulin coverage
o Pt may be subscribed supp or corrective doses of insulin in addition to
the basal/prandial insulin combination
 Helps elim use of sliding scale -> not very accurate
o Supplemental corrective insukni
 Can be used t cover episodes of hyperglycemia
 Should be combined with schedule BG measurements and
insulin admin
  Insulin dose is changes based on pts insulin sensitivity

HYPOGLYCEMIA MANAGEMENT:
 Important to monitor BG levels – if hypoglycemia is detected STOP ALL
INSULIN INFUSIONS
 In all cases of hypoglycemia: G must be assessed q15min UNTIL Bg has incr
to >70mg/dl
NURSING MANAGEMENT:
 Monitor Bg levels and insulin effectiveness, monitor hyperglycemia side
effects or vasopressor therapy, avoid hypoglycemia, provide nutrition and
educate family
MONITOR BG AND INSULIN EFFECTIVENESS AND AVOID HYPOGLYCEMIA
 Nurse is res for hourly monitoring of BG and titration of insulin infusion
according to hospital protocol while pt is hyperglycemic
  Nurses must have ongoing education about anabolic effect of insulin therapy
in critical illness
MONITOR HYPERGLYCEMIC EFFECTS OF VASOPRESSOR THERAPY
 Two vasopressors are commonly used as cont infusion to prevent hypotension
and raise BG levels – epi an nor epi
o Epi and norepi stim glucose production and suppress insulin secretion –
all lead to incr in Bg
PROVIDE NUTRITION
 When insulin is started, nutritional support is req
 Critical illness is associated with catabolism of skeletal muscle and this cause
inflammation and the endocrine stress response
 Feeding tube is rec as its associated with greater outcomes in critical illness
o Higher card content then TPN
 If eating is slowed = insulin must be adjusted to prevent hypoglycemia
COLLAB MANAGEMENT
 All disciplines concerned with endocrine status of pt should be involved in
measures to achieve target glucose control

DIABETES MELLITUS
 T1D: condition with loss of isulin from autoimmune dysfunction of beta cells
in pancreas
 T2D: insulin deficiency caused by progressive loss of insulin from the beta
cells and due to insulin resistance
DM DX
 DM diagnosed by measurement of FPG or by HA1c >6.5%
o FPG – 5.6mmol/l is normal fasting BG
o FPG – 5.6-6.9mmol/l is impaired FBG
o FPG: >7mmol/l is dx of diabetes
 Maintenance of lifestyle and diet is essential for T2D pts
 Glycated HA1c
o Maintaince of BG within target range is essential for ppl with DM
 GHA1c measures the percentage of glucose the RBCs have
absorbed from the plasma within the past 3 months
 Optimal target for pts with DM is A1c value <6.5%
T1DM
 Autoimmune disease that causes progressive destruction of beta cells in
pancreas
 Overtime auto-antibodies cause complete destruction and causes no insulin
to be produced – subsequent incr in BG
  Lack of insulin impairs card, fat and protein metabolism
MANAGING T1D:
 Iv or sq insulin – restores normal entry of insulin to cells
 Insulin can be long acting, basal, short acting and rapid
 Without insulin being controlled – DKA can occur and cause life threating
issues
T2DM:
 Decr insulin secretion and insulin resistance
 hyperglycemia occurs gradually
 trmt is through lifestyle changes and oral meds
Lifestyle management for T2DM
 weight reduction, incr exercise, diet
changes are essential
 diet of <30% of fat while incr
veggies, grains,
 medsto control BP, lower TAGS and
LDLs and treat CAD are needed
Pharmacological management fo T2D
 Meds are used when lifestyle changes
aren’t enough for reversing T2D
 Oral insulin antihyperglycemic meds
can be used – NOT INSULIN
 Metformin
o 1st line therapy for T2D
patients
o Makes insulin more sensitive
and suppress glucose
production
o Also causes peripheral gluc
uptake
o Can be combed with other
meds

 Sulfonylureas
o Oral meds that stim insulin secretion from pancreas
o Reduce A1c but 1-2% and have along acting duration
 Thiazolidinediones
o Increase sensitivity of muscle fat and liver cells to insulin
 DPP-4
o Incretin enhancers
 o Slow down degradation of GLP-1 (enzyme that prolongs gluc lowering
activity of GLP-1)
o Very low risk of hypoglycemia
 Sodium glucose cotransporter 2 Inhibitors
o These oral meds inhibit resorption of gluc in nephron by inhibiting renal
transporter SGLTS2
o Lower A1c slightly
o Can be used with other meds
o $$$
 GLP-1 Receptor Agonists
o Augment activyt of GLP-1
o Incr insulin secretion from pancreatic beta cells lower glucagon levels
and delay gastric emptying
o Not a replacement for insulin
 Alpha glucosidase inhibitors:
o Reduce postprandial hyperglycemi
o Taken at beginning of meal
o Lower a1c slightly

INSULIN IN T2DM
 Sometimes insulin is needed in D2M pts
 Pts with A1c>8&who are taking several antihyperglycemic meds
 LA insulin can be added bt this req more intensive BG monitoring
POLYPHARMACY IN DIABETES
 Polypharmacy can incr risk of med interactions and hypoglycemia – more
often seen in older adults
HYPERGLYCEMIC EMERGENCIES
 2 OF THEM – DKA AND HHS
 Hyperglycemia emergencies incl both DKA and HHS as they are very different
DKA:
 More common in T1D
 Dx criteria are
o BG >250mg.Dl
o Ph <7.3
o Serum bicarbonate <18mEq/L
 Severity of DKA dep on severity of metabolic acidosis and by presence of
altered mentation
 Infection most common cause of developing DKA
 Symptoms: fatigue polyuria, preceed DKA
 DKA can occur rapidly- within 24hrs
 Change sin insulin type or dosage, or incr metabolic demand can precipitate
DKA in pts with T2D
 Life cycle changes like growth spurts
 Ketoacidosis also occurs with acute pancreatitis
 Incr BG and acidosis, other signs are incr amylase and lipase – help
differentiate btwn DKA and pancreatitis
DKA PATHYPHYSIOLOGY
 Insulin deficiency
o Without insulin – gluc remains in blood and cells are starved
o Glucagon release from the liver incr BG and carbs and fats are broken
down to be converted into glucose
o ELEVATED SERUM LEVELS DO NOT DEFINE DKA
o Other critical factor is presence of ketoacidosis
 Hyperglycemia
o Incr plasma osmolality and blood becomes hyperosmolar
o Cell dehydration occurs as fluid is drawn from cells to bloodstream
o Dehydration stims catecholamines but this stims further
gluconeogenesis, lipolysis, and gluconeogenesis
 FVD:
o In normal circumstances insulin suppreses ketone manufacturing
o Ketoacidosis occurs when free FA are meta into ketones.
o In KA these ketones are produced more
o Blood tests measure ketones
o Bc ketones are excreted in urine, urine tests can be done
Acid-Base Balance:
 Varies dep on severity of DKA
 Mild DKA pH – 7.25-7.5
 Severe DKA pH can drop to below 7
 Serum bicarb also decr – consistent with KA dx
 Kussmaul resps start to kick in
FOCUSED PHYSX EXAM AND DX
 DKA has predictable clinical repress: malaise, PU/PD,
polyphagia—N/V/dehydration occur shortly after
 Pt with dka may be responsive or unresponsive dep on severity
 PE finds flushed pale skin, dry buccal membranes, decr skin turgor,
tachycardia and hypotension
 LAB STUDEIS
o Straightforward
o Presence of hyperglycemia, ketones, acidosis are rapid dx criteria for
DKA
MEDICAL MANAGEMENT
 After dx, rapid response is needed to reverse dehydration, replace insulin,
reverse ketoacidosis, and replenish E-
  Reversing dehydration
o Aggressive IVF therapy is needed
o Assessment of hydration is an important 1st step in treating DKA
o Isotonic normal saline is sued to replenish the vasc deficit and reverse
hypotension
 Insulin administration
o Mod-severe DKA – iv bolus of insulin at 0.1 unit for each kg of BW may
be admin
o Cont infusions of reg insulin is then given at 0.1unit/kg/ht
o When BG declines, insulin is decreased until steady BG is achieved
o Once Bg of ~11.1mmol/L is obtained acidosis and rehydration has
occurred insulin rate is reduced to 0.5unit/kg/hr
 Reversing ketoacidosis
o Replace fluid volume
o Adequate hydration and insulin correct acidosis and this trmt is
sufficient for many DKA pts
o Hyperglycemia is usually corrected before ketoacidemia
o Pts may req 6-9L of IVF
o Vol resus occurs over 24-36 hours
 Replenish E-
o Low serum K occurs with insulin admin before KA can be reversed
must be checked routinely – above 3.3mEq before insulin can be given
o Freq K+ checks are needed
o P+ levels can get low – sometimes replacement is recommended

NURSING MANAGEMENT OF DKA

 Admin fluids, insulin and E-
o Insulin is given iv forpts with serve dehydration or have poor peripheral
circ
o Rapid IVF is done via volumetric pump
o NPO until hyperglycemia is under control
o Goal is for BG to fall 50-70mg/dl
o COORD INVOLVED MONITORING BG, K AND ABGS HOURLY
o Insulin given SQ until BG, dehydration, hypotension and acid-base
balance are all normalized
 Monitoring response to therapy
o Acute I+Os are needed to monitor reversal of dehydration
o Hourly urine output iindicator for kidney function
o Vital signs, espec HR, hemodynamic values, and BP can assess fluid
replacement
o RR is checked for changes in rate, depth and acetone odour
o BG measured hourly
o TRANSITION SQ INSULIN: when lab values are stable and pt is more
alert – IV insulin is stopped and SQ is started
  Risk of hypo and hyperglycemia if too high or too low insulin SQ
is given
 Surveillance for complication
o FVE: from rapid fluid resus and can cause major issues if pts
cardiopulm or kidneys are compromised
 JVD, dyspnea w/o exertion, and crackle sin lungs are signs of FVE
 Reduce rate and vol of infusion, elevate HOB, give O2 may help
 Hourly urine outputs are mandatory to assess for kidney
function
o Hypoglycemia:
 Hosps have different protocols
 Dr nptified immediately and replacement gluc is given
 Unexpected behaviour changes, decr loc, diaphoresis and
tremors are all signs of hypoglycemia
o HYPO AND HYPERKALEMIA
 Hypokalemia can occur within first few hours of trmt due to
insulin admin
 Hyperkalemia occurs with acidosis or overaggressive k+
supplementation ‘
 Severe v arrythmias can occur if either condition occurs
o Hyponatremia
 Elim of Na from body causes osmotic diuresis and is wornseed
by V/D
 Signs: abd cramping, oHTN, behave changes
o LOC
 Cerebral edema can occur in pts with DKA
 Alterations in ots motor function, LOC, and mentation are signs
of incr ICP
 Neuro assessments done every hour or as needed during acute
ohases of rehydration and hyperglycemia
o Skin care: dehydration, hypovolemia, and hypophosphatemia all
interfere with o2 supply and reduce perfusion to skin – incr sus to
damage
 Reposition pts regularly
 Assess skin every couple of hours
o Oral care: toothbrushing and ensuring lips don’t crack is essential
o Infection prevention:
 Strict sterile technique is always used. Venipuncture sites are
checked q4 for signs of infection
o Pt and family education
 Teach ot target BG goals, hypo and hyper glycemia and its
harms, universal precautions must be emphasized for pts
handling
HHS
 Lethal complication of T2D
  Extremely high BG and osmotic diuresis
 KETOSIS IS ABSENT OR MILD
 Poorer outcomes bc many pts with T2D are obese or have comorbidities
 Occrs when pancreas cant produce sufficient amount of insulin
DX CRITERIA FOR HHS
 BG >600mg/dL
 Arterial pH >7.3
 Serum bicarb >18mEq/L
 Serum osmolality > 320 mmol/L
 Absent of mild ketonuria
Diff btwn HHS & DKA
 HHS is diff from DKA by presence of extremely high BG, more profound
dehydration, and absence of ketones
 Proteins and fats are also not used to create gluc in HHS  thus no ketotic
cycle is never started
HHS PATHOPHYS
 Deficit of insulin and excess glucagon
 Decr insulin prevents glucose from entering cells and stims glucagon
production that creates more gluc to enter blood
 HHS CAN EVOLVE OVER DAYS TO WEEKS
 Hemo conc persists despite removal of glucose form body via urine ‘
 Hyperosmolality and reduced blood volume stims ADH but ADH cant
overcome HHS state  worsens hypovolemia
 Hypovolemia: reduces perfusion to the kidney and oliguria occurs 
preserves water BUT causes glucose retention and hyperosmolality
 Epinephrine is excreted due to bodys stress and even more glucose enters
the bloodstream
 Dehydration and elevated BG may alter neuro function
FOCUSED PHYS ASSESSMENT AND DX
 Clinical signs:
o slow subtle onset, hx reveal malaise, blurred vision, PU/PD, weight loss
o Incr dehydration causes: mental confusion, convulsions, and coma
o PE may show signsof extreme FVD - longitudinal wrinkles in tongue,
decr salvation, and incr in HR and RR
 Lab studies
o Used to estab definitive dx of HHS
o BG >600mg/dl
o Serum osmolality >320mmol/L
o No acidosis
o Elavated HCT and depleted K and P
o Finger stick Bg testing is done at bedside
o Insulin regimen is decided by BG result
o Elevated BUN and Crea can indicate kidney impairment
o Acidosis MAY result from starvation ketosis or form incr lactic acid
production
 Medical management
o Rapid rehydration: physio saline is infused at 1l/hr
 Several liters may be needed to replace FVD and have BP and
CVP within normal range
  Hard to assess serum Na with severe hemoconc
o Insulin admin:
 Rec for HHS bc acidosis can occur if insulin is withheld
 Dep on pt bolus rates or cont rates of insulin can be used
o E replacement
 K and P can be lowered significantly with insulin admin
NJURSING GOALS FOR HHS
 Similar to those of DKA
 Admin fluids, insulin and E-, monitor response to therapy and provide pt
education