1. health and fitness
2. disease

1/15/2013
Beth Burgess, MHA, RHIA, CCS
Huff DRG Review Services
January 16, 2013
 CVA/TIA
 Respiratory
Failure
 Pneumonia
 Sepsis
 CHF
 AKI
Neurological deficits due to abnormality of the
vessels supplying the brain substance and
meninges
Clinical symptoms (TIA vs. Stroke)
Pathology (infarct vs. hemorrhage)
 Etiology (atherosclerosis; thrombosis; embolic)


1
1/15/2013
TIA


Stroke
Transient episode of
neurological dysfunction
caused by focal ischemia
to brain, spinal cord, or
retina without acute
infarction.
Lasts at least 30 seconds
and up to several days (3
days average).


Sudden neurological
deficit related to brain
necrosis caused by either
infarction (80%) or
hemorrhage (20%).
Strokes can be defined by
imaging studies or
persistent symptoms,
typically > 3 days.
 Acute/subacute
infarction on CT or MRI
on CT or MRI
 Significant neurological deficits persist at
time of discharge
 Hemorrhage
“Physician must link any abnormal imaging
study to the neurological condition”
Primary cause of CVA (ruptured intracerebral vessel)
Conversion of ischemic stroke
 Complication of thrombolytic therapy
 Tumor associated
 Trauma



Distinguish between traumatic vs. nontraumatic
(can be difficult even for clinician!)
2
1/15/2013
Obstruction of pre-cerebral arteries (carotid;
vertebrobasilar)
 Pre-cerebral artery occlusion > 70% is clinically significant

Physician must link occlusion to signs and symptoms
Obstruction of cerebral arteries

Cerebral artery embolism is suggested with neurological
symptoms without suggestion of pre-cerebral artery stenosis
and/or cerebral atherosclerosis.
Cerebral Embolus
Cerebral artery embolism is suggested with neurological
symptoms without suggestion of pre-cerebral artery stenosis
and/or cerebral atherosclerosis.

Recurrent TIAs or strokes usually different areas of the brain
(not always with same symptoms)

No significant obstruction of pre-cerebral vessels

No evidence of intracerebral atherosclerosis (small vessel
disease; old lacunar infarcts; atherosclerotic dementia;)
Sources of cerebral emboli:

Intra-arterial embolization from diseased pre-cerebral vessels

Cardiogenic (from the heart; aorta)
Cardiac Sources of Cerebral Emboli







Atrial fibrillation
Ventricular aneurysm
Cardiomyopathy
Prosthetic heart valves
Acute or subacute MI
Intimal injury from heart catheterization
PFO
3
1/15/2013
CCs



Hemiparesis
Acute confusion
Ischemic encephalopathy
MCCs

Brain
compression/herniation

Cerebral edema
Coma
Conversion hemorrhage



Patient with history of afib was admitted for
transient aphasia lasting 30 minutes. The
patient has a h/o afib but is not on any
medical treatment. TIA was diagnosed and
patient was treated with Lovenox and
Coumadin in the hospital then discharged on
Coumadin. The coder assigned TIA as the
PDX. Final DRG = 69.



Is there a potential for a different PDx?
If so, what?
Patient presented with transient right arm
weakness & numbness. Head CT showed no acute
infarcts. Carotid U/S showed 80% left carotid
stenosis. The final diagnosis was TIA. Patient is to
f/u for OP left carotid endarterectomy. The coder
assigned 433.10 (CAS) as the PDX. Final DRG = 68.

Is the PDx correct based on current documentation?
4
1/15/2013

Patient presented with slurred speech and leftsided weakness. The head CT report showed large
SDH with midline shift and vasogenic edema.
Patient was diagnosed with SDH and given IV
Decadron. The coder assigned 434.91 as the PDX
with dysphagia and left sided weakness as 2nd DXs.
Final DRG 66.


Is there a potential for a different DRG?
If so, what?
 Significant
impairment of gas exchange
work of breathing
 Intensive treatment
 Close monitoring
 Increased
Normal Lungs


Arterial blood PO2 < 60 mmHg.
Or
Arterial blood PCO2> 50mmHg
Pre-existing lung disease


Arterial pH < 7.35 w/ PCO2
>50mmHg***
Or
Change in baseline PO2 level
by 10-15mm
***generally more useful since
baseline PO2 not usually given.
5
1/15/2013
Work of breathing




Tachypnea (RR > 20)
Accessory muscle use
Moderate to severe
respiratory distress
SATs < 88%
Treatment




High flow oxygen (>4 to 6L
NC or non-rebreather
mask)
Controlled oxygen delivery
(i.e. Venturi mask) or low
flow in persons with CO2
retention
Noninvasive MV (BiPAP)
Invasive mechanical
ventilation with forced air
delivery via a tube in
airway

May be assigned as PDx when it is the condition established
after study to be chiefly responsible for occasioning
admission (CC 1st Qtr 2005)

Do not code acute respiratory failure as PDx when there is
a chapter-specific coding guideline (sepsis, obstetrics,
poisoning, HIV, newborn) or an alphabetic index or tabular
directive which takes precedence over the general
respiratory failure guidelines.
17

Patient with COPD on continuous home O2 at 2 L
presented with SOB. SATs on 2L were 75%. The
patient was placed on BiPAP, IV Solumedrol was
started and patient was admitted to the ICU for
acute on chronic respiratory failure due to COPD
exacerbation.

Can 518.84 be used as the PDx?
6
1/15/2013

Patient with no history of lung disease
presented with SOB. The patient was noted to
have accessory muscle use and was hypoxic with
SATs 87% on room air. ABGs showed PCO2 55.
The patient was admitted for acute respiratory
failure due to pneumonia. The patient was
admitted to telemetry on 4L and treated with IV
Azithromycin.


What is the appropriate PDx?
Patient was admitted for AECOPD with acute
respiratory distress. On admission the patient
had RR 20 with SATs 90% on room air. The patient
required O2 at 2L and IV steroids.

Would you query for acute respiratory failure?
Simple Pneumonia
Complex Pneumonia
Unspecified
Bacterial unspecified
Viral/Atypical/Mycoplasma
Strep or Hemophilus
Community Acquired
Healthcare associated
Nosocomial
Postobstructive
Immunocompromised host
Nursing home acquired
Specific bacteria**
Legionnares
Fungus/parasitic
Aspiration
Gram negative
7
1/15/2013
 The
treating physician must link any
positive cultures, gram stains, and
serological tests to the pneumonia before it
can be used to specify the pneumonia
 Positive cultures not required.
 Risk








factors
GERD
PEG tube
Bed bound
Advanced Parkinson’s
Advanced dementia
ETOH
abuse/intoxication
Seizure
Etc.
 ABX






Coverage
Clindamycin
Cefepime
Piperacillin (Zosyn)
Quinilones
Flagyl
Augmentin
*Check for swallow
study although does
not r/o aspiration.
 Pseudomonas
 E.
Coli
 Klebsiella
 Proteus
 Enterobacter
 Serratia
 Actinobacter
 Haemophilus
(DRGs 193-195)
8
1/15/2013
 Appropriate
antibiotic coverage (≥ 7 days)
And
 High risk host
And
 High risk for colonization
ABX Coverage
 Imipenem (Primaxin)
 Meropenem (Merem)
 Doripenem (Doribax)
 Ertapenem (Invanz)
 Cefepime (Maxipime)
 Cetazidime (Fortaz)
 Ciprofloxacin (Cipro)
 Levofloxacin (Levaquin)
 Piperacillin (Zosyn)
 Ticarcillin (Timentin)
 Tobramycin
 Gentamycin
 Aztreonam (Azactam)
NOT appropriate for gram
negative coverage:
 Penicillin
 Erythromycin
 Vancomycin
 Zithromax
 Clindamycin
 Zyvox
High risk host
High risk setting








Severe lung disease,
particularly with CF or
bronchiectasis
Chronic organ
dysfunctions such as CHF,
Cirrhosis, CKD
Diabetes
Malignancy
Immunosuppresive Rx
HIV
Alcoholics
Malnutrition



HCAP
Postobstructive
Bed confinement
9
1/15/2013

Certain types of pneumonia are designated clinically to
describe complex respiratory infections but are assigned to
pneumonia NOS unless specified as to potential organisms
being treated.

Hospital-Acquired or Institutional Acquired





HCAP; Nursing Home Acquired
Immunocompromised host
Gram negative; staphylococcal
Postobstructive (gram negative; anaerobes)
Community Acquired pneumonias (CAPs) are typically
Streptococcal, atypical, or Hemophilus influenza or viral.
Aspiration pneumonia can be community or hospital acquired.
Patients who develop pneumonia within 90 days of being
hospitalized in an acute care hospital for 2 or more days
should be approached as if they had hospital-acquired
pneumonia, as should residents of long-term care facilities,
hemodialysis patients, and patients who received intravenous
(IV) antibiotics, wound care, or chemotherapy within 30 days
of developing pneumonia.
HCAP
Hospital acquired
 Nosocomial
 Nursing home acquired
 Institutional acquired
 Pneumonia in immuno-compromised host


10
1/15/2013
Organisms:
Gram
see
negative bacilli
previous slides for organisms &ABX coverage
Anaerobic
bacteria
Any
of the drugs for gram negative or one of the
following: Clindamycin; Flagyl; Augmentin
Staphylococcus
Vancomycin;
aureus (particularly MRSA)
Zyvox; Bactrim; Tetracycline
Pneumonia that occurs as a result of bronchial
obstruction. Most commonly seen in patients
with bronchogenic carcinoma of lung.
Organisms:


Anaerobic bacteria
Gram negative bacilli
*Please refer to previous slides for antibiotic
coverage.

Patient has ESRD and several admissions over the
past 3 months and is now re-admitted for
pneumonia. The patient was treated with Zosyn
& Cipro for 5 days in the hospital and discharged
on both for 4 additional days.
 What type of pnuemonia does it appear is
being treated?
11
1/15/2013

Patient was admitted for pnuemonia. PMH is
notable for HTN, GERD and CHF. The patient
was treated with Clindamycin for a total of 7
days.
 What type of pnuemonia does it appear is
being treated?

Patient was admitted from the nursing home for
pnuemonia. The patient has a PMH of
hypothyroidism and CKD. The patient was
treated with 3 days of Azithromycin and
discharged back to the nursing home to continue
Azithromycin for 4 additional days.
 What type of pnuemonia does it appear is
being treated?

Patient recently began chemo for bronchogenic
carcinoma of the lung. The patient is now
admitted for postobstructive pnuemonia, which
was treated with Augmentin for 10 days.

What type of pnuemonia does it appear is being
treated?
12
1/15/2013
Systemic Inflammatory Response due to
Documented or suspected Infection
Without organ dysfunction
038.xx + 995.91
With organ dysfunction
038.xx + 995.92

3 or more of the following must be present and
cannot be explained by other disease process :














Fever (≥ 100.4) or hypothermia (≤ 96.8)
Leukocytosis (WBC >12), leukopenia (WBC < 4), bandemia (>
10% bands)
Tachycardia (HR >90)
Tachypnea (RR > 20)
Encephalopathy
Oliguria (<30cc/hr)
Hypotension
Increase Anion gap
Metabolic acidosis
Elevated lactate level
CRP elevation
Blood sugar >120 in a nondiabetic
DIC
Shock
 Compliance





issues
Diagnosis of sepsis without clinical support
Querying for sepsis without clinical support
Querying for sepsis when clinical indicators can
be explained by other disease process
Re-sequencing of PDx when complicaiton of
medical care
Bacteremia not indicator for SIRS!
13
1/15/2013

Patient presented with a painful leg with
erythema. The patient had temp 101, RR 18, HR
95,WBC 12.8, and elevated anion gap. The
patient was admitted for cellulitis of the leg and
treated with IV ABX.


Patient on 6 weeks of IV antibiotic treatment for
chronic osteomyelitis was admitted for infected
PICC line. The patient had hypotension, T100.8,
HR 120, RR 19, WBC 11.5. The patient was
admitted for infected PICC line and dehydration.



Is it appropriate to query for SIRS/sepsis?
What is the appropriate PDx?
Would it be appropriate to query for SIRS/sepsis?
Patient presented with acute confusion. The
patient had temp 95.4, HR 75, RR 17, WBC 18.5.
Head CT was negative. Urinalysis was positive.
The patient was admitted for metabolic
encephalopathy due to UTI.

Is it appropriate to query for SIRS/sepsis?
14
1/15/2013
Heart failure is a clinical syndrome resulting
from a failure of the heart to supply the body’s
need for circulation. This may be a structural
(valve) or functional (heart muscle weakness)
disturbance.

ETIOLOGY: Coronary artery disease; hypertension;
valvular; primary cardiomyopathy

ANATOMICAL: Left, right, or biventricular

TYPE (PHYSIOLOGICAL):
Diastolic only (preserved ejection fraction)
Systolic heart failure
Combined

ACUITY: Acute, chronic, or both
Left Heart Only***
 Left ventricular abnormal function
 Signs: Pulmonary congestion (effusion; edema)
Right due to Left (Combined)***
 Most common cause of Right HF is Left HF
 Signs: Pulmonary and peripheral congestion
 Abnormal left ventricular function with elevated RH pressures
Right Heart Failure Only
 Underlying lung disease or congenital heart disease with significant
shunting
 Signs of peripheral congestion: swollen liver; ascites; peripheral edema;
pleural effusions; Jugular vein distention
 Peripheral congestion with pulmonary hypertension and RV pressures with
normal Wedge pressure (Pulmonary venous pressures or PCWP)
***Represents 95% or more of HF
15
1/15/2013

Chronic cor pulmonale (not associated with left heart
failure)
 Intrinsic lung disease such as emphysema, COPD, ILD,
primary PAH
 Sleep apnea disorders
 Chronic pulmonary embolus

Acute cor pulmonale : acute pulmonary embolus
Pulmonary and tricuspid valve disorders
Peripheral AV shunts


Diastolic






No systolic dysfunction
Preserved Contractility
with EF>45%.
Ventricular end diastolic
pressures ELEVATED
(unless there is mitral
stenosis)
Cardiac output initially
normal or elevated
Left ventricular
hypertrophy present
Systolic




Decreased contractility
with EF<45%
Cardiac output
decreased
Ventricular end diastolic
pressures are elevated
Heart is dilated with
usually minimal or no
Left ventricular
hypertrophy
Everyone with systolic CHF has diastolic
dysfunction but not everyone with diastolic CHF
has systolic dysfunction.
MD has to document type of CHF. Cannot
assume!!!
16
1/15/2013
 Acute
only
(“compensated”)
 Acute on Chronic (“decompensated”)
 Unspecified
 Chronic

Symptoms & Signs: SOB, orthopnea, paroxysmal nocturnal
(PND), wheezing, and increased signs of peripheral
congestion (JVD, hepatomegaly, ascites, and peripheral
edema +/-.

Radiographic signs of volume overload
- Pulmonary vascular congestion
- pleural effusions (usually bilateral)
- interstitial edema
- pulmonary edema
- small pericardial effusions

Elevated BNP. This lab test if elevated only affirms the
patient has CHF. It should not be used to make the
diagnosis of acute CHF. Chronic CHF has an elevated BNP.
If BNP is not elevated this suggests patient may not have
CHF; however, there are few instances of where acute CHF
can occur without elevated BNP, particularly isolated right
heart failure.

Elevated LFTs; (alkaline phosphatase; SGOT/AST;
SGPT/ALT; bilirubin)

Decrease arterial oxygen levels (<97%; pO2<80mmHg)
17
1/15/2013
Treatment:





Intensification of any treatment regimen
Intravenous diuretic therapy
Intravenous vasodilators
Dialysis
Emergency cardioversion
Therapy
Left HF only
Right due to Left HF
ACE drugs/ARBs
X
X
Beta blockers
X
X
Diuretics
X
X
Lanoxin
X
X
Vasopressors
X
X
Vasodilators
X
X
Dialysis
X
X
Biventricular pacing
X
X
hBNP
X
X
Right only
X
X
Calcium channel Blockers
X
Viagra and related
compounds
X
MCC
CC
CHF NOS or any acuity
No Impact
X
Left HF NOS or any acuity
X
Right HF NOS or any acuity
X
Biventricular HF (NOS or any acuity)
X
Systolic (unspecified or chronic)
Systolic (Acute or acute on chronic)
X
X
Diastolic (unspecified or chronic)
Diastolic (Acute or acute on chronic)
X
X
S & D HF (unspecified or chronic)
S&D (Acute or acute or chronic)
X
X
18
1/15/2013
Ischemic
 Biventricular
enlargement
 Ejection fraction (EF)
decreased
 No LV hypertrophy;
only dilation of LV on
ECHO
Hypertensive
 Long standing HTN
 Left ventricular
hypertrophy prominent
on EKG/Echo
 Diastolic dysfunction
and/or preserved EF
(>45%) on Echo
 Enlargement is usually
confined to LV unless
ischemia and valve
disorders present
Acuity


Acute
Unspecified or chronic
Type
 Noncardiogenic (i.e. ARDS)
 Cardiogenic
- CHF
- Volume overload
Cardiogenic




Cause by increase
capillary hydrostatic
pressures
CHF: due to heart
dysfunction
(systolic/diastolic) and or
valvular heart disease
(ECHO abnormal)
Volume overload: no
cardiac dysfunction (i.e.
ESRD, TACO) ECHO normal
Elevated BNP
Non-cardiogenic




Caused by increased
permeability of alveolar
membrane
Direct injury caused by
infections, fatty emboli,
aspirations
Indirect injury due to
toxins such as in sepsis,
chemicals, etc.
BNP normal
19
1/15/2013



Volume/fluid overload is integral to CHF and not coded
separately unless MD says not due to heart failure. CC: 3rd
Qtr 1996; 2nd Qtr 2001
If a person is admitted for fluid overload due to missed
dialysis and has a h/o CHF, CHF is used as the PDx unless the
MD indicates fluid overload was not due to CHF. CC: 2nd Qtr
2001; 3rd Qtr 2007
Treatment of volume overload (pre-load reduction) is the
mainstay of treatment for ESRD patients. Dialysis is the
main mode of therapy acutely. This is the case regardless of
whether the patient has CHF or purely volume overload.

Acute pulmonary edema with heart disease is coded to CHF
unless the physician states the pulmonary edema is not
related.

If a person has an elevated BNP with LV dysfunction on Echo
clarify the nature of the volume overload.
TACO syndrome is a form of volume overload due to
transfusion. Acute pulmonary edema is not coded separately.

 Do
not code unspecified pulmonary edema
(514) as a CC if the cause is CHF. Pulmonary
edema is integral to CHF. If CHF or
acute/decompensated HF is not documented
you should try to clarify.
20
1/15/2013

Patient was admitted for acute GI bleed. The
patient has a PMH of GERD, HTN and CHF. Home
meds including Protonix, Lasix, Coreg &
Lisinopril were continued in the hospital. The
coder assigned 578.9 as the PDX with 428.0,
401.9 and 530.81 as ODXs. Final DRG was 379.
Is the final DRG correct based on current
documentation?
 Is there potential for a different DRG?


Patient was admitted for AKI from dehydration.
PMH includes DM, CHF and CAD. The patient was
aggressively hydrated with IVFs. On HD #2 the
patient developed SOB. CXR was ordered and
showed pulmonary congestion. Echo showed EF
25%. The patient was treated with IV Lasix. The
coder assigned 584.9 as the PDX with 428.0,
250.00 & 414.01 as ODXs. Final DRG was 684.
Is the final DRG correct based on current
documentation?
 Is there potential for a different DRG?


Patient with h/o COPD, HTN, CAD and systolic &
diastolic CHF presented with SOB & wheezing.
The admitting MD noted that CXR showed
pulmonary edema. The patient was admitted for
COPD and CHF. Treatment included IV
Solumedrol and IV Lasix. The coder assigned
491.21 as the PDX with 428.43 as an MCC. Final
DRG was 190.

Is the final DRG correct based on current
documentation?
21
1/15/2013
 Patient
with PMH of HTN, CKD IV and
diastolic dysfunction was admitted for CHF
exacerbation. Echo showed LVH, EF 65% and
no valvular disease. The coder assigned
428.33 as the PDX with 403.90 & 585.4 as
ODXs. Final DRG was 292.
Is the final DRG correct based on current
documentation?
 Is there potential for a different DRG?

Acute renal insufficiency –593.6- No CC
Acute kidney injury/failure- 584.9- CC
Acute tubular necrosis – 584.5- MCC
Vasomotor nephropathy – 584.5- MCC
Toxic nephropathy – 584.5- MCC
Acute interstitial nephritis – 580.89-MCC
Pre-renal azotemia – 790.6-No CC
Pre-renal failure – 788.99-No CC
Acute kidney disease –593.9- No CC
Renal failure unspecified – 586 – No CC
STAGE
Serum Creatinine
Urine Output
1
1.5 – 1.9 times baseline within 7 day
period
OR
> 0.3 mg/dl increase over 48 hrs.
<0.5 ml/kg/hr
for 6-12 hrs.
2
2.0 – 2.9 times baseline
<0.5 ml/kg/hr
for > 12 hrs.
3
3.0 times baseline
OR
Increase serum creatinine > 4.0mg/dl
OR
Initiation of renal replacement RX
<0.3 ml/kg/h
for > 24hrs.
22
1/15/2013
Increase SCr ≥ 0.3 over 48 hrs

Creatinine was 1.8 on admission and over the next 48
hours increased to 2.0. Does this patient have AKI?

Creatinine was 1.4 on admission and over the next 48 hrs
increased to 1.7. Does this patient have AKI?
Change in SCr ≥ 1.5 x baseline over 7 days

If CKD but no baseline documented:



Lowest SCr x 1.5 = ≥ highest SCr within 7 day period
 Ex: If SCr is 1.8 on admission it must decrease to a
minimum of 1.2 within 7 days. (1.2 x 1.5 = 1.8)
If no CKD documented then one would expect in a
normal person that the CKD would be < 1.0.
If baseline is documented on admission but SCr drops
below then the lowest SCr is new baseline.
Change in SCr ≥ 1.5 x baseline over 7 days

Patient admitted with dehydration. Creatinine noted on
admission to be 3.6. After rehydration patient was d/c on
day 5 with a creatinine of 1.8. Does this patient have AKI?

Patient with CKD was admitted with dehydration.
Creatinine noted on admission to be 1.3. After rehydration
patient was d/c on day 2 with a creatinine of 1.0. Does
this patient have AKI?
23
1/15/2013
Pre-renal
Intrinsic
Hypovolemia
Dehydration
Hemorrhage
Acute Tubular Necrosis (ATN)
Ischemia
prolonged dehydration
severe hypotension
Toxins
rhabdomyolysis
drugs (radio-contrast,
cisplatin, etc.)
Infection
pyelonephritis
Decrease in effective circulating
volume
Heart failure
Septic shock
Drugs
ACE-inhibitors/ARBs
NSAIDs
Post-renal
BPH
GU neoplasm
Bilateral ureteric stones
Glomerular
nephritis
collagen vascular disease
malignant hypertension
Renal Artery Atherosclerosis
renal artery stenosis
renal vein thrombosis
Interstitial
pyelonephritis
allergic intestinal nephritis
70
AKI/Pre-renal
AKI/ATN
U:P Osmolality
>1.4:1
1:1
U:P Creatinine
>50:1
<20:1
Urine Na (mEq/L)
<20
>80
FENa (%)
<1
>3
Urine Exam
Neg/hyalin casts
Granular casts
 Acute
kidney injury should be sequenced as
principal diagnosis instead of dehydration if
both are present on admission.
 Complication of transplant should be used if
acute renal failure occurs in a transplanted
kidney.
 Sepsis should be used as principal diagnosis if
acute renal failure is part of the SIRS or
infectious process.
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1/15/2013
 Patient
was admitted for PVD. Following
angiography the patient had a rise in
creatinine from 1.2 to 1.8 over 48 hrs.
Contrast induced nephropathy was
documented. Could the coder query for a
more specific type of kidney injury?
 Patient
has been on Bactrim for UTI as an OP.
The patient is now admitted for CHF. The
patient has CKD with a documented baseline
creatinine of 1.5. Creatinine on admission
was 2.0 and AKI was documented. Could the
coder query for a more specific type of
kidney injury?
 Patient
was admitted for CHF. On HD# 2 the
patient developed hypotension. Creatinine
increased from 1.5 on admission to 3.1.
Urinalysis showed granular casts. The
physician documented dehydration & AKI
from diuresis. Could the coder query for a
more specific type of kidney injury?
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1/15/2013
Please send any additional questions to:
[email protected]
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