Renal Emergency Revisi

RENAL
EMERGENCY
dr. Mega Elisa Hasyim

dr. Lutfy
Supervisor:
dr. Eva Delsi, Sp.EM
1
INTRODUCTION
Renal failure is a condition inability of the kidneys to perform
excretory function leading to retention of nitrogenous waste products
from the blood. Functions of the kidney are as follows:
• Electrolyte and volume regulation
• Excretion of nitrogenous waste
• Elimination of exogenous molecules, for example, many drugs
• Synthesis of a variety of hormones, for example, erythropoietin
• Metabolism of low molecular weight proteins, for example, insulin
• Acute and chronic renal failure are the two kinds of kidney failure.
2
Acute Renal Failure (ARF)
ARF is the syndrome in which

glomerular filtration declines
abruptly (hours to days) and is
usually reversible.
3
AKI can be diagnosed with any one of the following:
(1) creatinine increase of 0.3 mg/dL in 48 hours,
(2) creatinine increase to 1.5 times baseline within last 7 days,

or
(3) urine volume less than 0.5 mL/kg per hour for 6 hours.
4
Chronic Renal Failure (CRF)
CRF or chronic kidney disease (CKD) is defined as a persistent impairment

of kidney function, in other words, abnormally elevated serum creatinine for
more than 3 months or calculated glomerular filtration rate (GFR) less than
60 ml per minute / 1.73m2. It often involves a progressive loss of kidney
function necessitating renal replacement therapy (dialysis or
transplantation).
When a patient needs renal replacement therapy, the condition is called end-
stage renal disease (ESRD).
5
CKD classified based on grade:
Grade of CKD GFR
Grade 1 greater than 90
Grade 2 60 to 89
Grade 3a 45 to 59
Grade 3b 30 to 44
Grade 4 15 to 29
Grade 5 Less than 15
6
EPIDEMIOLOGY
Indonesian Renal Registry

7
8
9
HYPERKALEMIA
• The severity of hyperkalemia is related to plasma potassium. The rapidity of

the development to hyperkalemia has a significant bearing on clinical
severity. Do not wait for the potassium level result to come back from the lab
if either clinical state or ECG suggest hyperkalemia; rather treat empirically.
• Clinical manifestation can be protean. Metabolic acidosis and hypocalcaemia

can worsen the severity of hyperkalemia
10
The severity of hyperkalemia
SEVERITY POTASSIUM LEVEL ECG
Mild <6.0 mmol/L
ECG may be normal or show only peaked T
waves
Moderate 6.0 - 7.0 mmol/L
ECG may show peaked T waves
Severe 7.0 - 8.0 mmol/L
ECG show flattering of P wave and QRS with T
wave (sine wave) that leads to atrioventricular
(AV) dissocation, ventricular dysrhythmias, and
death
11
12
Four step Management of
Hyperkalemia
Step 1: Stabilization of membrane potential
• Administer ca gluconate 10%: 10-20 ml IV over 3-10 minutes, to
maximum of 20 ml.
Step 2: Shift the potassium in extra-cellular

fluid into the intra-cellular fluid
• Administer dextrose/insulin: 40-50 ml D50 IV over 5-10 minutes and
10 IU of regular insulin as separate boluses.
• Administer sodium bicarbonate 1 mEq/kg body weight IV as bolus
over 5 minutes in patients with moderate to severe metabolic
acidosis; repeat in half an hour in patient with severe metabolic
acidosis.
• Administer salbutamol: Add 5 mg salbutamol to 3-4 ml saline and
nebulize over 10 minutes.
13
Four step Management of
Hyperkalemia
Step 3: Remove potassium from the body
• Resonium A: 15 g orally (PO) 4-6 hourly.

• Haemodialysis (contact Renal Medicine first)
Step 4: Prevent further potassium increase
• Review all medication, e.g. Span K, ACE inhibitors, and

beta blockers
• Review diet and give advice
Repeat a serum potassium level to ensure there is no continued increase in potassium and an
improvement in the potassium level,
14
15
RENAL FAILURE
• Acute renal failure: An abrupt (within 48 hours) reduction

in kidney function:
• An absolute increase in serum creatinine of ≥ 26.4 mol/L
• A percentage increase in serum creatinine of ≥50% from the

baseline level
• A reduction in urine output (documented oligouria of <0.5 ml/kg per
hour for >6 hours)
16
• Chronic kidney disease
• Structural kidney damage or decrease kidney function (decreased
glomerular filtration rate, GFR) for ≥3 months
• End-stage renal disease (kidney failure)

• The GFR is < 15 ml/min per 1.73 m2, which is accompanied in most
case by sign and symptoms of uremia, or
• A need to start kidney replacement therapy (dialysis or
transplantation).
17
Chronic Renal Failure with Fluid
Overload and not on Dialysis
Manage the patient in the critical care area
Place the patient in an upright position
Administer supplemental high flow oxygen
Monitoring ECG, vital sign q 5 to 10 minutes, and pulse oximetry
Preserve one upper-limb vessel for future arteriovenous, access

(no blood taking or drip setting)
18
Drug therapy
GNT 0.5 mg sublingually (SL) or nitroderm patch 5-10 mg
or IV 10-200 μg/min
Morphine 2-5 mg IV (if there is severe pulmonary

oedema)
Felodipine 2.5 mg PO if blood pressure is high
Furosemide 120-240 mg IV
Conceder dialysis if there is severe fluid overload,

hyperkalemia, metabolic acidosis, or the patient is not
responding to the above measures (contact the renal
physician-on-call)
19
Coronary Renal Failure with Fluid Overload
without Accessible Peripheral Venous Access
GNT 0.5 mg SL or nitroderm patch 5-10 mg
Felodipine 2.5 mg PO if blood pressure is high
Furosemide 120-240 mg PO
20
SEVERE METABOLIC
ACIDOSIS
• Patient often present with non-specific symptoms> its
clinical effects are overshadowed by the signs and symptoms
of the underlying disorder
• Metabolic acidosis should be suspected in any patient with

hyperventilation, altered mental state, and haemodynamic
instability
21
Management
The patient should be managed in the critical care area
Ascertain airway patency and manage accordingly
Monitoring: ECG and vital sign q 5 to 10 minutes
Establish peripheral IV access with normal saline at ‘keep open’ rate
Labs: Full blood count, urea/electrolytes/creatinine, stat capillary blood

glucose, arterial blood gas, serum osmolality, urinalysis, and ECG
X-ray: No specific role in acid base states. However, a kidney, ureter, and
bladder X-ray may be useful to identify and ingested substance
22
Specific Therapy
• Bicarbonate therapy is reversed of severe organic acidosis or
those not easily revered. The goal is to raise the arterial pH >7.2.
There is no need to correct the pH if it is ≥7.2 unless there is some
life-threatening problem that need to be addressed.
• Formula: Dose of NaHCO3 [mEq] = (Desired [HCO3-] –

Measured [HCO3-] x 50% body weight in kg. Half this dose is
given initially with the remainder depending on repeat laboratory
evaluation.
23
• Dosage: Bolus therapy is recommended only for those with
severe acidosis or when there is haemodynamic compromise.
Patient with less life-threatening acidosis may be treated with IV
1 L of D5% and run over 1-2 hours with repeated arterial blood
gases as guide to therapy.
• Potential complication of the therapy are hypernatremia,

hyperosmolality, volume overload, hypokalemia, and post
treatment alkalosis
24
Acute Pulmonary
Oedema
SIGNS:
• The patient is usually severely breathless,

sweaty, nauseated and anxious.
• Initially they may have a dry or

productive cough (sometimes with pink,
frothy sputum).
• Patients may also develop paroxysmal

nocturnal dyspnoea or orthopnoea.
25
HISTORY:
• Check for a past history of

relevant conditions - eg,
coronary heart disease, valvular
heart disease, diabetes.
• Review current medication.
• Ask about smoking and alcohol

use.
26
SIGNS:
• Respiratory distress, pale, sweaty, tachypnoeic and tachycardic.
• Cyanosed, have evidence of congested neck veins and a raised JVP.
• Basal/widespread rales or fine crackles
• Oxygen saturation is usually <90% on room air.
• Assess for a gallop rhythm (3rd heart sound) and murmurs suggestive of
valve stenosis or regurgitation.

• Hypotension - the triad of hypotension (systolic blood pressure <90 mm
Hg),
• Hypertensive heart failure, a high blood pressure, tachycardia and
vasoconstriction present with signs of pulmonary oedema without extensive
systemic congestion.
• Where pulmonary oedema occurs in association with right heart
failure, hepatomegaly and peripheral oedema are usual.
27
INVESTIGATION:
• Blood tests:
• Renal function, electrolytes, glucose, cardiac enzymes, LFTs, clotting tests (INR).
• Arterial blood gases and pH.
• ECG: look for evidence of arrhythmia, myocardial infarction or other
cardiac disease - eg, left ventricular hypertrophy.

• CXR: to exclude other causes of breathlessness and confirm pulmonary
oedema.
• Echocardiogram: transthoracic echocardiography is usually adequate.
• A urinary catheter enables accurate measurement of urinary output,
which helps rapidly to assess diuretic response and fluid balance.

• More invasive procedures are required for intensive support, including
arterial and central venous pressure lines and pulmonary artery catheters.
28
GOAL
The goals of therapy are to improve oxygenation, maintain an adequate blood

pressure for perfusion of vital organs, and reduce excess extracellular fluid.
The underlying cause must be addressed.
29
30
VENTILLATORY
NITRAT DIURETICS SUPPORT INOTROPES
The mechanism of nitrate action is smooth muscle relaxation,

causing venodilatation and consequent preload reduction at low
doses. Higher doses cause arteriolar dilatation, resulting in
reduced afterload and blood pressure. Specifically in the coronary
arteries, this dilatation results in increased coronary blood flow.
These actions
collectively improve
oxygenation and reduce
the workload of the
heart.
31
VENTILLATORY
Recommended Nitrate Dose Regimens

Presentation and
Dose Frequency Max dose
administration
Glyceryl trinitrate spray 400 microgram (2 puffs) repeat every 5 min 1200 mcg
Glyceryl trinitrate 300–600 microgram repeat every 5 min 1800 mcg
sublingual tablet
Glyceryl trinitrate 5–10 microgram per min double every 5 min 200 mcg per min
intravenous infusion*
* first line in acute pulmonary oedema
32
VENTILLATORY
Nitrates are associated with hypotension and

therefore blood pressure monitoring is essential
to ensure the systolic blood pressure is
maintained above 90 mmHg. They should not
be given if the systolic blood pressure is less
than 90 mmHg or the patient has severe aortic
stenosis, as these patients are preload dependent. If the patient has
recently taken a phosphodiesterase inhibitor, such as sildenafil, nitrates
are contraindicated.
33
VENTILLATORY
However, diuretics are

indicated for patients with
evidence of fluid
overload. Loop diuretics such
as furosemide reduce preload
and should be withheld or
used judiciously in patients
who may have intravascular
volume depletion.
34
VENTILLATORY
Recommended Doses of Furosemide

Presentation and Dose Frequency
administration
Slow intravenous bolus 4 mg/min repeat after 20 min if
necessary
– normal renal function 40–80 mg –
– renal insufficiency or up to 160–200 mg –
severe heart failure
– chronic loop diuretic initial intravenous dose –
users equal to maintenance oral
dose,* titrate to response
Intravenous infusion 5–10 mg per hour continuous
* The oral bioavailability of furosemide (frusemide) is approximately half that of the intravenous
formulation.
35
VENTILLATORY
The first step in improving ventilation for patients

with acute pulmonary oedema is to ensure that they
are positioned sitting up. This reduces the ventilation–
perfusion mismatch and assists with their work of
breathing.
If required, oxygen should be administered to achieve

a target oxygen saturation of 92–96%.
For patients with chronic obstructive pulmonary
disease, the target oxygen saturation is 88–92%
36
VENTILLATORY
4 L/minute via nasal cannulae,
5–10 L/minute via mask,
15 L/minute via a non-rebreather reservoir mask or
high-flow nasal cannulae with fraction of inspired

oxygen greater than 35%.
37
VENTILLATORY
If the patient has respiratory distress, acidosis

or hypoxia, despite supplemental oxygen,
non-invasive ventilation is indicated. There is
no significant clinical benefit of bi-level
positive airway pressure ventilation (BiPAP)
over continuous positive airway pressure
ventilation (CPAP), so the modality chosen
should be guided by local availability.
38
VENTILLATORY
If, despite non-invasive ventilation,

there is persistent hypercapnia,
hypoxaemia or acidosis, then
intubation should be
considered. Other indications for
intubation include signs of physical
exhaustion, a decreasing level of
consciousness or cardiogenic shock.
39
VENTILLATORY
Intravenous inotropic drugs are indicated in acute pulmonary

oedema when there is hypotension and evidence of reduced
organ perfusion. The first-line therapy is an intravenous
infusion of dobutamine.
40
INDICATIONS FOR DIALYSIS
• Severe pulmonary oedema
• Severe uncontrollable hypertention from severe fluid overload not

responding to diuretic
• Hyperkalemia refractive to medial treatment
• Severe metabolic acidosis refractive to medical treatment
• Some poisoning, e.g. methanol, ethylene glycol, and salicylates (severe)
• Uremia, including pericarditis and encephalophaty
41
PROBLEMS ASSOCIATED
WITH DIALYSIS
Haemodialysis • Neurological dysfunction
• Vascular access-related complication • Dialysis disequilibrium
• Bleeding Peritoneal dialysis
• Loss of thrill in shunt • Peritonitis
• Infection
• Leaking catheter
• Non-vascular access-related
• Hypotension
complication
• Hypotension • Acute abdomen
• Dyspnea • Infection
• Chest pain
42
Presentasi Kasus
43
1 Patient
st
44
Triage
Identitas • Ny. S, Perempuan, 55 tahun
Airway: • Paten, Clear
• Nafas spontan, RR 30 x/menit, SDV (+/+), RBH , + +

Breathing: + +
RBK (-/-) wheezing (-/-)
+ +
• Akral hangat, HR 77 bpm regular, SpO2 99% NRM
Circulation:
15 lpm, TD 190/85
GCS: • E4V5M6
GDS • 250
Triage: • P1
45
Anamnesis
(Alloanamnesis dengan keluarga pasien 8 Desember
2019)
Pasien rujukan dari RS Amanah. Pasien mengeluh

sesak napas dalam melakukan aktifitas ringan
sejak 1 bulan SMRS makin lama makin memberat.
Pasien tidur dengan 2-3 bantal. Pasien dirawat di
RS Amanah selama 1 minggu, keluhan sesak napas
sempat membaik namun memburuk 1 hari SMRS.
Pasien sering mengonsumsi Rheumacyl dan

Oskadon bila merasa tidak enak badan. Pasien
membelinya di warung tanpa resep dokter
46
RPD:
• Riwayat keluhan yang sama disangkal
• Riwayat darah tinggi disangkal
• Riwayat DM disangkal
• Riwayat stroke disangkal
• Riwayat penyakit ginjal disangkal
RPK
• Riwayat DM saudara kandung pasien
47
Anamnesis Sistem
Cerebrospinal Kardiovaskuler
• Demam (-), kejang (-), sakit kepala • Jantung berdebar (-), nyeri dada
(-), kepala berputar (-), hemiparese (-), hipertensi (-)
(-), sulit bicara (-)
Respirasi Gastrointestinal
• Batuk (-), pilek (-), sesak napas (+) • Mual (-), diare (-), sulit BAB (-),
sejak 1 bulant terakhir BAB darah (-)
Urogenital
• BAK keruh (-)
48
Pemeriksaan Fisik
Kepala Leher
Kepala: Mesosefal Cor
Mata: CA +/+, pupil isokor I : IC tak kuat angkat
3mm/3mm, reflex cahaya (+/+) P: IC
Mulut : mukosa basah P: batas jantung kesan tidak
Leher : JVP 8 cm, pulsasi A.
karotis teraba kuat
melebar
A: BJ I II tunggal, murmur (-),
gallop (-)
Abdomen
I: datar
A: BU + normal Pulmo
P: timpani, pekak berlih (-) I: pengembangan dada kanan = kiri
P: Supel, NT (-), hepar lien tidak P: fremitus raba kanan = kiri
teraba membesar P: sonor/sonor
A: SDV: +/+,
Ekstremitas RBH + +
Akral dingin Edem + +
+ +
- - - -
RBK -/-, Wheezing -/-
- - + +
49
Pemeriksaan Penunjang
(Lab Darah di RS PKU Muhammadiyah Gombong tanggal 8 Desember 2019)
Pemeriksaan Hasil Nilai Rujukan Satuan

Hematologi
Darah Lengkap
Leukosit 13.64 H 3.6-11 rb/ul
Eritrosit 4.18 3.8-5.2 juta/L
Hemoglobin 12.1 11.7-15.5 gr/dl
Hematokrit 35.6 35-47 %
MCV 85.3 80-100 sL
MCH 28.9 26-43 pg
MCHC 33.8 32-36 g/dl
Trombosit 380 150-440 rb/ul
Hitung Jenis
Basofil% 0.2 0.0-1.0 %
Eosinofil% 0.2 L 2.0-4.0 %
Neutrofil% 95.7 H 50.00-70.0 %
Limfosit% 2.4 L 25.0-40.0 %
Monosit% 1.5 L 2.0-8.0 %
Kimia
Diabetes
GDS 211 H 70-105 mg/dl
50
Faal Ginjal
Ureum 338 H 15-39 mg/dl
Creatinin 15.99 H 0.6-1.1 mg/dl
Faal Hati
Albumin 3.88 3.5-5.0 g/dL
SGOT 29.70 0-35 u/l
SGPT 35.20 H 0-35 u/l
Analisa Gas Darah
PH 7.0 L 7.35-7.45
PCO2 15.1 L 35-45 mmHg
PO2 212.0 H 80-105 mmHg
HCO3 3.3 L 22.0-26.0 mmol/l
O2 Saturasi 99.0 75.00-99.00 %
BE -27.2 -3.00 – 3.00 mmol/l
Kesimpulan AGD: Asidosis metabolik kompensasi sebagian
Elektrolit
Natrium 138.5 135-147 mEq/L
Kalium 6.95 H 3.5-5.0 mEq/L
Imuno Serologi
Anti HIV Non Reaktif Non Reaktif
HBs Ag Negative Negative
51
EKG
Irama : normosinus
Frekuensi: 72 bpm
P interval: 0.16 detik
QRS kompleks: 0.08 detik
QT interval: 0.32 detik
Posisi: semi vertical
Aksis: 60O
Zona transisi: -
ST depresi di lead I aVL

T tall V3-V6
52
Diagnosis
Acute Lung Oedem,

Hiperkalemia, Asidosis
Metabolik ec CKD stage 5
CHF NYHA IV
53
Tatalaksana di
Monitoring
IGD
IVFD NS lifeline Kondisi umum, GCS
NRM 15 lpm Vital sign
Furosemide 60 mg IV ECG
NTG 20 cc / jam IV RBH
Ceftriaxon 1 gr IV Urin output
Ca Gluconas 1 gr IV
D40 50 ml IV
Insulin 10 IU IV
DC
HD Cito
54
Follow Up
55
Minggu, 8/12/2019 DPH 0
S O A P
Sesak napas KU: tampak sakit berat • Acute Lung • NRM 15 lpm
GCS: E4V5M6 Oedem • IVFD NS 20 tpm
TD: 84/50 • CHF • Inj. Furosemide 5
HR: 195 NYHA IV mg/jam
RR: 30 • CKD • Inj. Ceftazidim 3 x 1 gr
Suhu: afebris • Inj. Amiodaron 150 mg
bolus 10 menit
Mata: CA +/+, SI -/- • Lanjut Amiodaron 150
Cor: BJ I II reg, intensitas mg habis dalam 8 jam
normal, bising -
Pulmo: SDV +/+, RBH + +
• Furosemid 1 x 20 mg
RBK -/-, Whz -/- + +
PO
+ +
Abdomen: Supel, NT -, • OMZ 2 x 40 mg PO
BU + normal
Ext: akral hangat, CRT <
2
edem
- -
+ +
56
Senin, 9/12/2019 DPH 1
S O A P
Sesak napas KU: tampak sakit berat • CHF • Facemask 5 lpm
sudah GCS: E4V5M6 NYHA IV • IVFD NS 20 tpm
berkurang TD: 100/50 • CKD on • Inj. Furosemide 5
HR: 190 HD mg/jam
RR: 26 • Inj. Ceftazidim 3 x 1 gr
Suhu: afebris • Inj. Amiodaron 3 x 150
mg
Mata: CA +/+, SI -/- • Inj. Ca Glukonas 1 gr
Cor: BJ I II reg, intensitas (ekstra)
normal, bising -
Pulmo: SDV +/+, RBH - -
• Furosemid tab 1 x 20 mg
RBK -/-, Whz -/- - -
PO
+ +
Abdomen: Supel, NT -, • OMZ 2 x 40 mg PO
BU + normal • Bicnat 3 x 500 mg PO
Ext: akral hangat, CRT < • Pro renal 1 x 1 tab
2
edem
- -
+ +
57

Hematologi
Darah Lengkap
Eritrosit 3.11 L 3.8-5.2 juta/L
Hemoglobin 9.1 L 11.7-15.5 gr/dl
Hematokrit 25.9 L 35-47 %
MCV 83.4 80-100 sL
MCH 29.2 26-43 pg
MCHC 35.0 32-36 g/dl
Kimia
Diabetes
GDS 88 70-105 mg/dl
Faal Ginjal
58
Selasa, 10/12/2019 DPH 2
S O A P
Lemes KU: tampak sakit sedang • CHF NYHA • Pindah bangsal
GCS: E4V5M6 IV • Nasal Kanul 2 lpm
TD: 170/80 • CKD on HD • IVFD NS 20 tpm
HR: 80 • Inj. Ceftazidim 3 x 1 gr
RR: 22
Suhu: afebris • Furosemid tab 1 x 20 mg
Mata: CA +/+, SI -/- PO
Cor: BJ I II reg, intensitas • OMZ 2 x 40 mg PO
normal, bising - • Bicnat 3 x 500 mg PO
Pulmo: SDV +/+, RBH -/-, • Pro renal 1 x 1 tab
RBK -/-, Whz -/- • Vit K 3 x 10 mg PO
Abdomen: Supel, NT -, BU • Kalnek 3 x 500 mg PO
+ normal • Plan HD 11/12/19
Ext: akral hangat, CRT < 2
edem
- -
+ +
59
Kimia
Diabetes
GDS 88 70-105 mg/dl
Faal Ginjal
Elektrolit
Natrium 135.0 135-147 mEq/L
Kalium 4.49 3.5-5.0 mEq/L
60
Rabu, 11/12/2019 DPH 3
S O A P
Lemes KU: tampak sakit berat • CHF NYHA • HD
GCS: E4V5M6 IV • Nasal Kanul 2 lpm
TD: 110/80 • CKD on HD • IVFD NS 20 tpm
HR: 80 • Inj. Ceftazidim 3 x 1 gr
RR: 22
Suhu: afebris • Furosemid tab 1 x 20 mg
Mata: CA +/+, SI -/- PO
Cor: BJ I II reg, intensitas • OMZ 2 x 40 mg PO
normal, bising - • Bicnat 3 x 500 mg PO
Pulmo: SDV +/+, RBH -/-, • Pro renal 1 x 1 tab
RBK -/-, Whz -/- • Vit K 3 x 10 mg PO
Abdomen: Supel, NT -, BU • Kalnek 3 x 500 mg PO
+ normal • Tranfusi PRC 1 kolf
edem
- -
+ +
61
Hematologi
Darah Lengkap
Eritrosit 2.27 L 3.8-5.2 juta/L
Hemoglobin 6.6 L 11.7-15.5 gr/dl
Hematokrit 19.1 L 35-47 %
MCV 83.4 80-100 sL
MCH 29.0 26-43 pg
MCHC 34.4 32-36 g/dl
Faal Ginjal
62
USG Upper-Lower Abdomen
(RS PKU Muhammadiyah Gombong 12 Desember 2019)
Kesimpulan
• Hydronefrosis dextra grade 5
• CKD sinistra
• Tak tampak kelainan pada organ hepar, VF, lien, pancreas,

vesica urinaria
63
Kamis, 12/12/2019 DPH 4
S O A P
pusing KU: tampak sakit berat • CHF NYHA • Nasal Kanul 2 lpm
GCS: E4V5M6 IV • IVFD NS 20 tpm
TD: 180/70 • CKD on HD • Inj Ceftazidim 3 x 1 gr
HR: 80 • Furosemid tab 1 x 20 mg
RR: 20 PO
Suhu: afebris
• OMZ 2 x 40 mg PO
Mata: CA +/+, SI -/- • Bicnat 3 x 500 mg PO
Cor: BJ I II reg, intensitas • Pro renal 1 x 1 tab
normal, bising - • Vit K 3 x 10 mg PO
Pulmo: SDV +/+, RBH -/-, • Kalnek 3 x 500 mg PO
RBK -/-, Whz -/- • ISDN 2 x 5mg
Abdomen: Supel, NT -, BU • Digoxin 1 x 1 mg
+ normal • Candesartan 1 x 8 mg
Ext: akral hangat, CRT < 2 • Amlodipin 1 x 10 mg
edem • As Folat 1 x 1
• Tranfusi PRC 1 kolf
- -
- -
64
Jumat, 13/12/2019 DPH 5
S O A P
nyeri perut KU: tampak sakit berat • CHF NYHA • Nasal Kanul 2 lpm
TD: 110/70 • CKD on HD • Inj. Ceftazidim 3 x 1 gr
HR: 80 • Furosemid tab 1 x 20 mg
RR: 20 PO
Suhu: afebris
• OMZ 2 x 40 mg
Mata: CA +/+, SI -/- • Bicnat 3 x 1
Cor: BJ I II reg, intensitas • Pro renal
normal, bising -
Pulmo: SDV +/+, RBH -/-,
RBK -/-, Whz -/-
Abdomen: Supel, NT
epigastrium, BU + normal
edem
- -
- -
65
Sabtu, 14/12/2019 DPH 5
S O A P
nyeri perut KU: tampak sakit berat • CHF NYHA • Nasal Kanul 2 lpm
berkurang GCS: E4V5M6 IV • IVFD NS 20 tpm
TD: 120/70 • CKD on HD • Furosemid tab 1 x 1
HR: 80 • Ceftazidim 3 x 1
RR: 20 • OMZ 2 x 40 mg
Suhu: afebris
• Bicnat 3 x 1
Mata: CA +/+, SI -/- • Pro renal
Cor: BJ I II reg, intensitas • Vit K 3x1
normal, bising - • Kalnek 3x1
RBK -/-, Whz -/-
Abdomen: Supel, NT
epigastrium, BU + normal
edem
- -
- -
66
Minggu, 15/12/2019 DPH 5
S O A P
- KU: tampak sakit berat • CHF NYHA • Nasal Kanul 2 lpm
TD: 120/70 • CKD on HD • Furosemid tab 1 x 1
HR: 80 • Ceftazidim 3 x 1
RR: 20 • OMZ 2 x 40 mg
Suhu: afebris
• BLPL
Mata: CA +/+, SI -/-
Cor: BJ I II reg, intensitas
normal, bising -
RBK -/-, Whz -/-
Abdomen: Supel, NT -, BU
+ normal
edem
- -
- -
67
2 Patient
nd
68
Triage
Identitas • Tn. S, Laki-laki, 60 tahun
Airway: • Paten, Clear
• Nafas spontan, RR 36 x/menit, SDV (+/+),- RBH

- ,
Breathing:
RBK (-/-) wheezing (-/-) + +
+ +
• Akral dingin, HR 110 bpm regular, SpO2 99% NRM

Circulation:
10 lpm, TD 111/57
GCS: • E2V1M3
GDS • 272
Triage: • P1
69
Anamnesis
(Alloanamnesis dengan keluarga pasien 8 Desember 2019)
Keluhan utama: sesak napas
Pasien merupakan rujukan dari RS PKU Muhammadiyah

Sruweng, Pasien merasakan sesak napas memberat sejak 3 hari
yang lalu. Semakin memberat hingga sesaat sebelum SMRS.
Sesak napas tidak dipengaruhi oleh aktivitas. Tidak membaik
saat istirahat. Sesak hingga masuk rumah sakit belum
berkurang dan belum diberi obat apapun. Riwayat asma, sakit
jantung, batuk lama, dan demam disangkal. Saat sampai di
rumah sakit pasien mengalami penurunan kesadaran,
disorientasi, tidak dapat merespon panggilan pemeriksa. Pasien
telah dirawat di RS PKU Sruweng selama 1 hari.
70
RPD
• Pasien pernah mengalami sesak serupa, lalu berobat ke
dokter. Oleh dokter di diagnosa dengan CKD grade V,
dan mendapat rekomendasi untuk melakukan HD 2 kali
seminggu. Pasien telah melakukan HD sebanyak 2 kali,
namun karena mengetahui creatinine sudah turun, pasien
menghentikan sendiri pengobatan HD nya. Terakhir
pasien melakukan HD sekitar 1 bulan yang lalu di RS
PKU Gombong.
• Riwayat sakit jantung disangkal
• Riwayat alergi obat disangkal
• Riwayat asma disangkal
• Riwayat hipertensi: (+) tidak terkontrol obat
RPK
71
Anamnesis Sistem
Cerebrospinal Kardiovaskuler
• Demam (-), kejang (-), sakit kepala • Jantung berdebar (+), nyeri dada
(-), kepala berputar (-), hemiparese (-), hipertensi (+) sejak 7 tahun
(-), sulit bicara (-) yang lalu
Respirasi Gastrointestinal
• Batuk (-), pilek (-), sesak napas (+) • Mual (-), diare (-), sulit BAB (-),
memberat sejak 3 hari terakhir BAB darah (-)
Urogenital
• BAK keruh (-)
72
Pemeriksaan Fisik
Kepala Leher
Kepala: Mesosefal Cor
Mata: CA +/+, pupil isokor I : IC tak kuat angkat
3mm/3mm, reflex cahaya (+/+) P: IC
Mulut : mukosa basah P: batas jantung kesan tidak
Leher : JVP 6 cm, pulsasi A.
karotis teraba kuat
melebar
A: BJ I II tunggal, murmur (-),
gallop (-)
Abdomen
I: datar
A: BU + normal Pulmo
P: timpani, pekak berlih (-) I: pengembangan dada kanan = kiri
P: Supel, NT (-), hepar lien tidak P: fremitus raba kanan = kiri
teraba membesar P: sonor/sonor
A: SDV: +/+,
Ekstremitas RBH- -
Akral dingin Edem + +
+ +
+ + - -
+ + + + RBK -/-, Wheezing -/-
73
Diagnosis
Acute Lung Oedem
CKD grade V
Hiperkalemia
74
PEMERIKSAAN PENUNJANG
EKG Saat di Sruweng
75
76
Hasil laboratorium darah di RS PKU Sruweng
Lab darah tanggal 7 desember 2019

Darah rutin
Hb 8,9 g/dl
AL 11.690/mm3
AE 2.94 jt/mm3
Hct 26%
AT 163.000/mm3
Gol. Darah A
Kimia darah
Ureum 204.5 mg/dl
Creatinine 13.69
GDS 132 mg/dl
Imunoserologi
HBsAg Non reaktif
77
EKG saat admission di IGD
78
79
Tatalaksana di RS
Tatalaksana di RS
PKU
PKU Sruweng
Muhammadiyah
• O2 NRM 15 lpm • Dikarenakan GCS pasien
• IVFD NaCl 0,9% lifeline semakin turun, dan terjadi
• Furosemide 60 mg/8 jam desaturasi, maka pasien
• NTG 1 ampul + D5% 10% direncanakan padang ETT.
• Rencana ETT dengan
• Amlodipine 1x10 mg
premed
• Irbesaartan 1x150 mg • Ketamin
• Bicnat 3x1 • Artakurium
• CaCo3 3x1 • Furosemid 60 mg
• Pasang DC
80
Monitoring
Monitoring dilakukan pada tanggal 08/12/19, pukul 17.00
 S: penurunan kesadaran, GCS E2V1M3, tampak sesak
 O:
 TD: 110/57 RR : 36-40 x/m SiO2 : 92-95% NRM 10 lpm
 HR: 111 x/m reguler T : 36.9
 A: Dyspneu e.c Acute lung oedem dengan riwayat CKD grade V tidak terkontrol HD
 P:
 O2 NRM 10 lpm
 Inf. NaCl 0,9% lifeline
 Rencana intubasi, pasang ETT no. 7 dengan premedikasi
 Premedikasi dengan:
 Atrakurium 25 mg
 Ketamin
 Saat intubasi, terjadi apneu dan cardiac arrest  algoritma cardiac arrest
81
• Evalua
si:
tidak
teraba
RJP 5 nadi • Evalua
Siklus dan si:
18.05 tidak Tidak
ada teraba
napas, nadi
RJPirama
5 siklus dan
assitol
18.08 napas. • Evalua
Irama si:
asistol tidak
teraba • Evalua
RJPEphine
• 5 siklus
phrine nadi si:
18.10
1 mg dan tidak
napas. teraba
Irama nadi
RJPasistol
5 siklus dan
Irama si:
asistol tidak
RJPEpinep
• 5 siklus teraba
hrine 1 nadi • Evalua
18.15
mg dan si:
napas. tidak
Irama teraba
RJPasistol
5 siklus nadi
18.18 dan
napas
• Epinep
hrine 1
ROSC
mg
18.20
82
EKG Setelah ROSC
83
84
Hasil laboratorium darah di RS PKU Gombong

Darah rutin
Hb 8,3 g/dl
AL 14.91 rb/ul
AE 2.75 jt/mm3
Hct 24.6%
AT 228.000/mm3
Gol. Darah A
Hitung jenis
Basofil 204.5 mg/dl
Eosinofil 13.69
Neutrofil 132 mg/dl
Limfosit 5.7
Monosit 3.7
Kimia
GDS 191
85
Hasil laboratorium darah di RS PKU Sruweng

Kimia darah
Ureum 281 mg/dl
Creatinine 15.51
Elektrolit
Na 137.3
K 8.56
86
Monitoring
Monitoring post ROSC pukul 18.25
 S: KU: penurunan kesadaran GCS: E1V1M1, post ROSC

 O:
 TD : 220/90 RR : 32-36 x/m SiO2 : 100% ETT
 HR : 102 x/m reguler T : 35.4
 Thorax: Cor : BJ1-BJ2 regular
Pulmo : SDV +/+, Rk +/+, Whezing -/-
 GDS: 272 mg/dl
 A: Post ROSC e.c Cardiac arrest
 P:
 Terpasang ETT no. 7
 Drip Norepinephrine 0,5 mcg/kgbb/menit
 Inf. NaCl 0,9% lifeline
 Koreksi hiperkalemi
 Ca glukonas 1 amp, D40% 2 flacon, Insulin 10 IU IV bolus
87
Konsultasi DPJP
Konsul dr. Haryono, SpPD
• Advice dr. Haryono, SpPD:
• HD Cito dengan resep
• QB : 180
• RD : 500
• UF qnd : 200
• Rawat ICU
• Transfusi PRC 2 kolf on HD
• NE dilanjutkan
88
Monitoring
Monitoring post ROSC pukul 19.30
• S: KU: penurunan kesadaran GCS: E1V1M1
• O:
• TD : 136/62 RR : 16-18x/m SiO2 : 89% ETT
• HR : - x/m reguler T : 35.7
• Thorax: Cor : BJ1-BJ2 regular

• A: Cardiac arrest
• P:
• Algoritma cardiac arrest sesuai ACLS 2015
89
• Evalua
si:
tidak
teraba
RJP 5 nadi • Evalua
Siklus dan si:
19.30 tidak Tidak
ada teraba
napas, nadi
RJPirama
5 siklus dan
assitol
Irama si:
asistol tidak
teraba • Evalua
RJPEphine
• 5 siklus
phrine nadi si:
19.35
1 mg dan tidak
napas. teraba
Irama nadi
RJPasistol
5 siklus dan
Irama si:
asistol tidak
RJPEpinep
• 5 siklus teraba
hrine 1 nadi • Evalua
19.40
mg dan si:
napas. tidak
Irama teraba
RJPasistol
5 siklus nadi
19.43 dan
napas
• Epinep
hrine 1
ROSC
mg
19.45
90
Monitoring
Monitoring post ROSC kedua pukul 19.45
• S: KU: penurunan kesadaran GCS: E1V1M1, post ROSC kedua
• O:
• TD : 108/52 RR : 22-24 x/m SiO2 : 100% ETT
• HR : 74 x/m reguler T : 35.2

• A: Post ROSC e.c Cardiac arrest
• P:
• Terpasang ETT no. 7
• Drip Norepinephrine 0,5 mcg/kgbb/menit
• Inf. NaCl 0,9% lifeline
91
Monitoring
• S: KU: penurunan kesadaran GCS: E1V1M1
• O:
• TD : 96/48 RR : 16-18 x/m SiO2 : 90% ETT
• HR : - x/m reguler T : 35.4
Pulmo: SDV +/+, Rk +/+, Whezing -/-
• A: Cardiac arrest
• P:
• Algoritma cardiac arrest sesuai ACLS 2015
92
• Evalua
si:
tidak
teraba
RJP 5 • Evalua
nadi
Siklus dan si:
tidak Tidak
20.40 teraba
ada
napas,
RJP 5 nadi
irama
siklus dan
napas. • Evalua
assitol
20.43 si:
Irama
asistol tidak
RJP 5
• Ephine teraba
siklus nadi
phrine
120.45
mg dan
napas.
Irama • Epinep
Defibrilasi
VT hrine 1 • Evalua
150 joule
mg si:
tidak
RJP 5 teraba
siklus nadi • Evalua
20.50 dan si:
napas. tidak
Irama
RJP 5 teraba
asistol
siklus nadi
20.53 dan
napas,
irama
Defibrilasi • Epinep
150VTjoule hrine 1 • Evalua
20.55 mg si:
tidak
RJP 5 teraba
siklus nadi
20.58 dan
Pasien dinyatakan
napas,
meninggal
irama
dihadapan
asistole
petugas dan
keluarga
21.00
93
Approach to Patient
94
Approach to Patient
(Subjective)
Theory Patient 1 Patient 2

Chief complaint Breathlessness for over a Patient start to breathless
Acute dyspneu (Sudden onset of month since 3 days before
extreme breathlessness) admission
Anxiety Yes Decrease of awareness
Productive cough Sometime Initially with cough
For a month Lack of activity because
Dyspneu d’Effort shortness of breathe
Yes Cannot answer the
Breathless to speak examiner question
Feel like drowning Yes
Swollen foot For a month Since inadequate
hemodialysis
Chest pain Not present Not present
95
Approach to Patient
(Subjective)

Patient history - Patient diagnosed with CHF
History of heart disease (coronary since 1 year ago
heart disease, valvular heart disease)
Hitory of kidney disease - -
History of respiratory illnesses - Patient also diagnosed with CKD
since 1 month ago
Lack of information
History of metabolic disease (diabetes, - Lack of information
metabolic syndrome)
History of surgery (valve surgery, - Theres no surgery history
tumor excision)
Medical history (current medication) Often take NSID without Amlodipin 1x10 mg, irbesartan
doctor’s advice 150 mg, simvastatin 1x80, as.
folat 1x1
History of allergic to drugs or food - Lack of information
History of bad intake/habit (smoking - Patient not smoking since
or alcoholism) diagnosed with CHF
96
Approach to Patient
(Subjective)

Family history - -
History of heart disease
(coronary heart disease, valvular
heart disease)
History of metabolic disease - -
(diabetes, metabolic syndrome)
History of allergic to drugs. food, - -
or environment
History of bad intake/habit - -
(smoking or alcoholism)
97
Approach to Patient
(Objective)

General survey
Decrease of awareness GCS E4V5M6 GCS when admission is
E2V1M3
Pale Yes Look extremely pale (body
and extremity)
Sweaty Yes Sweating on body
Vital sign
Tachypnoe RR 30 x/min RR 36-40 x/min
Tachycardia HR 71 bpm HR 110 bpm
Decrease of SpO2 SpO2 before oxygenation SpO2 before oxygenation
90% 85%
Hypertension 190/85 mmHg 111/57 mmHg
98
Approach to Patient
(Objective)

Physical examination
Cyanosed - Look pale
Increase of JVP JVP 5 + 4 cmH2O JVP +/- 6
Basal/widespread rales or fine RBH RBH
crackles + + + +
+ + + +
+ + + +
RBK (-/-) RBK (-/-)
Right heart failure association: Hepatomegali (-) Lack of examination
hepatomegaly peripheral Peripheral oedema (+)
oedema
Gallop (3rd heart - There’s no third sound or
sound)/murmurs murmur
99
Approach to Patient
(Objective)
Supporting examination Normosinus rhythm HR 72 bpm
ECG: evidence of arrhythmia, Position: semi vertical Sinus rhythm 75x/m with PVC,
myocardial infarction, left ventricular Axis: 60O LAD
hypertrophy ST depression in lead I and aVL
T tall V3-V6
Laboratory finding
Blood glucose GDS 211 mg/dl H GDS 272 mg/dl H
Kidney disease analysis (ur/cr) Ur 338 1 mg/dl H Ur 281 mg/dl H
Cr 5.99 mg/dl H Cr 15.51 mg/dl H
Blood gas & pH abnormality Partially compensated Lack of examination
metabolic acidosis
Imbalance electrolyte Na 138.5 mEq/L Na 137.3 mEq/L
K 6.95 mEq/L H K 8,56 mEq/L H
CXR No CXR examination No CXR examination
A – alveolar oedema (bat’s wing)
B – kerley B line
C – cardiomegaly
D – dilated prominent upper lobe
vessel
E – pleural effusion
100
Approach to Patient
(Assessment)

Assessment • Acute Lung Oedem ec Dyspneu e.c acute lung
CKD grade V oedem dd CHF with CKD
• CHF NYHA IV grade V uncontrolled by
hemodyalisis
101
Approach to Patient
(Managament)

Nurse in sitting position Fowler position Supine position
IV line IVFD NS lifeline IVFD NaCl 0,9% lifeline
High flow concentration O2 NRM 15 lpm NRM 10 lpm; intubation
planning
Deuretics Furosemide 60 mg -
Nitrat NTG 20 cc / jam -
Inotropics drugs to augment cardiac - Norepinephrine 0,5
function mcg/kg/min
Urine output monitors 800 cc/24 jam (0.5 cc/kg/jam) DC
Electrolytes correction Ca Gluconas 1 gr IV Ca Gluconas 1 gr IV
D40 50 ml IV D40 50 ml IV
Insulin 10 IU IV Insulin 10 IU IV
102
Summary
• Worsening of renal function can developing renal emergencies that contributes to long-
term kidney dysfunction, potentially leading to end-stage kidney disease (ESKD).
• The most frequent causes of CKD include hypertensive kidney disease, Diabetic
nephropathy, and primary glomerulopathies
• Hyperkalemia, metabolic acidosis, renal failure and acute lung oedema may occur in
renal emergencies
• The initial focus should be on the evaluation and management of the ABCs (airway,
breathing, and circulation) of the patient. Providers should use proper laboratory and
imaging studies as well as ECGs to further evaluate for electrolyte disturbances and
other metabolic cardiac sequel of disease.
103

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RENAL

dr. Mega Elisa Hasyim

• Electrolyte and volume regulation

• Excretion of nitrogenous waste

• Elimination of exogenous molecules, for example, many drugs

• Synthesis of a variety of hormones, for example, erythropoietin

• Metabolism of low molecular weight proteins, for example, insulin

ARF is the syndrome in which

(1) creatinine increase of 0.3 mg/dL in 48 hours,

(2) creatinine increase to 1.5 times baseline within last 7 days,

CRF or chronic kidney disease (CKD) is defined as a persistent impairment

Indonesian Renal Registry

• The severity of hyperkalemia is related to plasma potassium. The rapidity of

• Clinical manifestation can be protean. Metabolic acidosis and hypocalcaemia

Step 2: Shift the potassium in extra-cellular

• Resonium A: 15 g orally (PO) 4-6 hourly.

Step 4: Prevent further potassium increase

• Review all medication, e.g. Span K, ACE inhibitors, and

• Acute renal failure: An abrupt (within 48 hours) reduction

• A percentage increase in serum creatinine of ≥50% from the

• End-stage renal disease (kidney failure)

Place the patient in an upright position

Administer supplemental high flow oxygen

Monitoring ECG, vital sign q 5 to 10 minutes, and pulse oximetry

Preserve one upper-limb vessel for future arteriovenous, access

Morphine 2-5 mg IV (if there is severe pulmonary

Felodipine 2.5 mg PO if blood pressure is high

Conceder dialysis if there is severe fluid overload,

GNT 0.5 mg SL or nitroderm patch 5-10 mg

Felodipine 2.5 mg PO if blood pressure is high

• Metabolic acidosis should be suspected in any patient with

Ascertain airway patency and manage accordingly

Monitoring: ECG and vital sign q 5 to 10 minutes

Establish peripheral IV access with normal saline at ‘keep open’ rate

Labs: Full blood count, urea/electrolytes/creatinine, stat capillary blood

• Formula: Dose of NaHCO3 [mEq] = (Desired [HCO3-] –

• Potential complication of the therapy are hypernatremia,

• The patient is usually severely breathless,

• Initially they may have a dry or

• Patients may also develop paroxysmal

• Check for a past history of

• Review current medication.

• Ask about smoking and alcohol

• Cyanosed, have evidence of congested neck veins and a raised JVP.

• Basal/widespread rales or fine crackles

• Oxygen saturation is usually <90% on room air.

valve stenosis or regurgitation.

vasoconstriction present with signs of pulmonary oedema without extensive

failure, hepatomegaly and peripheral oedema are usual.

• Arterial blood gases and pH.

• ECG: look for evidence of arrhythmia, myocardial infarction or other

cardiac disease - eg, left ventricular hypertrophy.

• A urinary catheter enables accurate measurement of urinary output,

which helps rapidly to assess diuretic response and fluid balance.

The goals of therapy are to improve oxygenation, maintain an adequate blood

The mechanism of nitrate action is smooth muscle relaxation,

Recommended Nitrate Dose Regimens

* first line in acute pulmonary oedema

Nitrates are associated with hypotension and

However, diuretics are

Recommended Doses of Furosemide

The first step in improving ventilation for patients