DEPARTMENT OF ANAESTHESIOLOGY

AND CRITICAL CARE

Kulliyyah Of Medicine
International Islamic University Malaysia (IIUM)

Case Write-up ICU

Year 4 Block 1, 18/19

TITLE:
Septic Shock Secondary to
Hospital Acquired Pneumonia

Name : Hannah Nahdia Mohammed Fauzi

Matric Number : 1516864
Group : C4
Supervisor : Asst. Prof. Dr. Suhaila Nanyan
IDENTIFICATION DATA

Name : Harun Bin Chik

Age : 75 Years Old

Gender : Male

Race : Malay

Religion : Islam

Registration Number : 1006063

Identification Card Number : 430105115038

Address : Kg. Belukar, Batu 3, 25150 Kuantan.

Marital Status : Married

Ward : General Intensive Care Unit (GICU)

Date of Admission : 19/11/2018

Date and Time of Death : 21/11/2018, 3.53pm

CASE SUMMARY

My patient, Encik Harun, a 75-year-old Malay male, ADL dependant, housebound for the
last 3 years, with underlying COAD was recently discharged from IIUMMC on the 2 nd of
November 2018 after a 2-week admission for AECOAD secondary to community
acquired pneumonia (CAP). On his last admission, a CT brain was done showing
multifocal infarcts of varying ages. A CT Thorax was also done in view of widened
mediastinum; film showed elevated right hemidiaphragm indicative of phrenic nerve
palsy and minimal consolidative changes which were likely infective in origin.

Since discharge, he has been having on and off fever associated with intermittent
coughing. He has also had poor oral intake since discharge which had worsened
drastically for the past three days. He became non-verbal and had reduced
consciousness since 2.00pm today and then went into respiratory distress at 3.30pm.
He was brought to ED IIUMMC by his daughter where his GCS was recorded to be
E1V2M5 (8/15) with hypotension and desaturation under room air. ECG taken showed
sinus rhythm with premature ventricular contraction (PVC) and poor R wave
progression. He was given fluid resuscitation and eventually BP picked up to 135-
151/103-124 mmhg. He was then prepared for intubation in view of worsening
respiratory distress and for airway protection in view of drop in GCS. Post intubation it
was noted that his BP dropped down to 40/31mmHg and was pulseless at 5.45 pm. CPR
was commenced with adrenaline given once during the first cycle, subsequently he
developed unstable VT requiring defibrillation twice at 6.01 pm and 6.03 pm with ROSC
at 6.04 pm. BP recorded at that time was 108/81 mmhg, PR: 120 bpm (total down time
was 20 mins). He was then started on Noradrenaline infusion running at 14 mls/hr.

At 10.22pm that day, he was admitted to ICU as planned. He was to be invasively

monitered and continue noradrenaline infusion to keep MAP>65mmHg.
MANAGEMENT AND PROGRESSION IN ICU

Day 1 of ICU Admission (18/11/2018)

At 2220 hours, my patient was admitted to the GICU ward from ED via whole bed.
Upon arrival to ICU, patient was sedated and intubated with GCS 2T/15 (E1VTM1), both
pupils 2mm and sluggish to light, both upper and lower limbs were not responsive.
Patient is currently ventilated with SIMV VC mode, FiO 2:0.5, PEEP:12, Rate:12, PS:6.
Patient had a central line at his left femoral with ongoing drip; 5th pint normal saline for
maintenance, IV Midazolam run at 2mls/hour, IV Fentanyl run at 2mls/hr, IVI
Noradrenaline 8mg/50cc D5% run at 0.28mcg/kg/min equal to 14.1mls/hr. He had
ongoing correction IVI calcium gluconate and IVI magnesium sulphate. Patient was
intubated with ETT size 8mm, anchored at 21cm, pressure cuff 28cmH20. CBD intact
size 18Fr with poor urine output. Peripheral line intact size 20G at left leg. Intake from
ED: 2400mls, output: 30mls. Patient hemodynamically recorded NIBP:92/55mmHg, HR
124bpm, RR 22/min, SpO2 100% and DXT 5.3mmol/L.

He was also given IV Tazosin in view of his septic shock and IV Hydrocortisone.

Day 2 of ICU Admission (19/11/2018)

NUTRIC score: 9 
SOFA score: 12

Patient is on day 2 of IV Tazosin, still in septic shock. His inotropic support is unable to
be weaned down as MAP is only around 65-69mmHg. Otherwise, he is afebrile with
reducing TWC (21  15) and his latest temperature is 36.1.

Approach Comments

Airway - ETT is a must for patients with

- Patient intubated with ETT size 8 GCS<8 in order to maintain patent
and anchored at 21cm, pressure airway and facilitate mechanical
cuff 28cmH2O ventilation

Breathing - CPAP is a form of positive airway

- Bibasal crepitations on pressure ventilator, which applies
auscultation mild air pressure on a continuous
- Ventilated on CPAP PS mode, basis to keep the airways
FiO2: 0.5, Pressure Support: 6, continuously open in people who are
 PEEP: 8
- SpO2: 100% under FiO2 0.5
- ABG: 7.29/19/130/12.5
- CXR: Fibrotic changes seen
bilaterally, widened
mediastinum, no obvious
haziness or consolidation seen.
Circulation
- BP: 77/70 mmHg (MAP 72)
- PR: 111 bpm
- DRNM
- Lactate 5.6
- Noradrenaline 0.33 mcg/kg/min
and Vasopressin 0.02 unit/min
Disability
- GCS E1VTM4 (5T/15)
- Pupils 2/2 bilaterally reactive
- Riker’s score -2 (Sedated with IV
Midazolam 1mg/hr and IV
Fentanyl 20mcg/hr)
Electrolytes
- Na: 149
- K: 4.3
- Cl: 114
- Ca/Mg/PO4: 1.99/ 1.16/ 1.57
Fluids
- IVD Hartmann’s Solution 1 pint
over 24 hours
Gastrointestinal
- NBO since admission
- Novasource renal 10 mls/hour
- BSL 8.3 not on STAR
Nonspecific Therapy
not able to breathe spontaneously on
their own.
- PEEP of 5-7 is best for maintaining
lung volume
- ABG shows metabolic acidosis
- Patient is hemodynamically unstable;
hypotensive, tachycardic
- The lactate is high in septic shock due
to global hypoperfusion causing the
patient to be in a hypoxic state thus
being under anaerobic conditions, the
production of lactate is increased.
- Metabolic acidosis
- GCS shows no eye opening response,
T indicates patient is ventilated and
patient moves to pain stimulus, not
improving from yesterday
- Riker’s score -2 indicates that patient
is very sedated; arouses to physical
stimuli but does not communicate or
follow commands
- Electrolyte monitoring is important
as patient is in septic shock
- Hypernatremia and hyperchloremia
is indicative of hypovolaemia
- HS is given to correct the patient’s
electrolyte imbalance
 F- Novasource renal 10 H- 30 degrees F- IVD HM 1 pint over 24
mls/hour U- IV Ranitidine 50mg tds hours
A- Fentanyl infusion 20 G- As above I- As above
mcg/hour D- not indicated for dialysis
S- Midazolam infusion D- Reviewed and served
1mg/hour L- Left femoral quad lumen
T- nil day 2, arterial line right
radial day 2, NG tube right
nostril day 2, CBD day 2 (all
clean and not inflamed)
E- As above

Day 3 of ICU Admission (20/11/18)

NUTRIC score 9
SOFA score 14  15 (Platelet reducing to 140, Bilirubin increasing to 42)

Patient is still intubated and ventilated on SIMV FiO2: 0.35, Rate: 8, Pressure Support:
12, PEEP: 8, SpO2: 100% under FiO2 0.35. Patient was changed from CPAP to SIMV; it
allows the patient to breath spontaneously between mandatory tidal volume delivered
by the machine. Lactate decreased from 5.6 to 3.2 showing improvement despite it still
being high. Patient is now on triple inotropes (Noradrenaline, Vasopressin and
Dobutamine) and dose of Vasopressin was increased to 0.04 unit/min. Patient’s current
GCS is E2VTM4 (6T/15). He is still given IVI Fentanyl 20mcg/hour, IVI Midazolam was
stopped. Novasource renal now given 20mls/hour.

Patient was escalated down from IV Tazocin to IV Meropenem due to high PCT. Patient
also started on IV Thiamine. Total white cell has further decreased to 13.5.

Day 4 of ICU Admission (21/11/18)

NUTRIC score 9
SOFA score 14  15  17 (Worsening respiratory and renal component)

On routine review, the patient was noted to become more hypotensive despite on triple
inotropic support. Cardiac monitoring showed pulseless electrical activity (asystole)
hence CPR was commenced at 3.20pm. He was also given IV Adrenaline 1mg, IV
NaHCO3 100mls, IV Calcium Gluconate 10mmol. Patient ROSC at 3.28pm.

A family conference was carried out and it was explained to the family members
regarding the patient’s current condition 
- Septic shock with multiorgan failure 
- Patient currently critically ill with severe lung infection, poor heart function,
worsening kidney function and history of CVA 
The family members understood the situation and were not keen for CPR 

Cardiac monitoring showed asystole at 3.53 pm 

Pulse was not palpable, BP unrecordable , Pupils 5/5 non-reactive 

Cause of death : Septic shock secondary hospital acquired pneumonia with multiorgan
failure 

DISCUSSION
Modes of Mechanical Ventilation

Volume Modes
- Assist-Control Ventilation (ACV)
o Also known as continuous mandatory ventilation (CMV). Each breath is
either an assist or control breath, but they are all of the same volume.
o The larger the volume, the more expiratory time required.
o If the I:E ratio is less than 1:2, progressive hyperinflation may result.
o ACV is particularly undesirable for patients who breathe rapidly – they
may induce both hyperinflation and respiratory alkalosis. Note that
mechanical ventilation does not eliminate the work of breathing, because
the diaphragm may still be very active.
- Synchronized Intermittent-Mandatory Ventilation (SIMV)
o Guarantees a certain number of breaths, but unlike ACV, patient breaths
are partially their own, reducing the risk of hyperinflation or alkalosis.
o Mandatory breaths are synchronized to coincide with spontaneous
respirations.
o Disadvantages of SIMV are increased work of breathing and a tendency to
reduce cardiac output, which may prolong ventilator dependency. The
addition of pressure support on top of spontaneous breaths can reduce
some of the work of breathing. SIMV has been shown to decrease cardiac
output in patients with left-ventricular dysfunction.

Pressure Modes
- Pressure-Controlled Ventilation (PCV)
o Less risk of barotrauma as compared to ACV and SIMV.
o Does not allow for patient-initiated breaths.
o The inspiratory flow pattern decreases exponentially, reducing peak
pressures and improving gas exchange
o The major disadvantage is that there are no guarantees for volume,
especially when lung mechanics are changing. Thus, PCV has traditionally
been preferred for patients with neuromuscular disease but otherwise
normal lungs
- Pressure Support Ventilation (PSV)
o Allows the patient to determine inflation volume and respiratory
frequency (but not pressure, as this is pressure-controlled), thus can only
be used to augment spontaneous breathing.
o Pressure support can be used to overcome the resistance of ventilator
tubing in another cycle (5 – 10 cm H20 are generally used, especially
during weaning), or to augment spontaneous breathing. PSV can be
delivered through specialized face masks.
- Pressure Controlled Inverse Ratio Ventilation (PCIRV)
 o Pressure controlled ventilatory mode in which the majority of time is
spent at the higher (inspiratory) pressure.
o Early trials were promising, however the risks of auto PEEP and
hemodynamic deterioration due to the decreased expiratory time and
increased mean airway pressure generally outweight the small potential
for improved oxygenation
- Airway Pressure Release Ventilation (APRV)
o Airway pressure release ventilation is similar to PCIRV – instead of being
a variation of PCV in which the I:E ratio is reversed, APRV is a variation of
CPAP that releases pressure temporarily on exhalation.
o This unique mode of ventilation results in higher average airway
pressures.
o Patients are able to spontaneously ventilate at both low and high
pressures, although typically most (or all) ventilation occurs at the high
pressure.
o In the absence of attempted breaths, APRV and PCIRV are identical. As in
PCIRV, hemodynamic compromise is a concern in APRV. Additionally,
APRV typically requires increased sedation

Tube Compensation
- Positive End Expiratory Pressure (PEEP)
o Note: PEEP is not a ventilatory mode in and of itself
o Does not allow alveolar pressure to equilibrate with the atmosphere.
PEEP displaces the entire pressure waveform, thus mean intrathoracic
pressure increases and the effects on cardiac output are amplified. Low
levels of PEEP can be very dangerous, even 5 cm H20, especially in
patients with hypovolemia or cardiac dysfunction.
o PEEP is indicated clinically for
 Low-volume ventilation cycles
 FiO2 requirements > 0.60, especially in stiff, diffusely injured
lungs such as ARDS and 3) obstructive lung disease.
o Do NOT use in pneumonia, which is not diffuse, and where PEEP will
adversely affect healthy tissue and worsen oxygenation. One way to gauge
the effect of PEEP is to look at peak inspiratory pressure (PIP) – if PIP
increases less than the added PEEP, then the PEEP improved the
compliance of the lungs.
- Continuous Positive Airway Pressure (CPAP)
o Positive pressure given throughout the cycle. It can be delivered through
a mask and is can be used in obstructive sleep apnea (esp. with a nasal
mask), to postpone intubation, or to treat acute exacerbations of COPD
Septic Shock
Sepsis 3 definition of sepsis is the life-threatening organ dysfunction due to a
dysregulated host response to infection.
 Sepsis clinical criteria: organ dysfunction is defined as an increase of 2 points or
more in the Sequential Organ Failure Assessment (SOFA) score [Figure 1]
o For patients with infections, an increase of 2 SOFA points gives an overall
mortality rate of 10%
 Patients with suspected infection who are likely to have a prolonged ICU
stay or to die in the hospital can be promptly identified at the bedside
with qSOFA (“HAT”); i.e. 2 or more of:
o Hypotension: SBP less than or equal to 100 mmHg
o Altered mental status (any GCS less than 15)
o Tachypnoea: RR greater than or equal to 22

Figure 1: SOFA Score

Figure 2: qSOFA Score

Septic shock is a subset of sepsis in which underlying circulatory and cellular or
metabolic abnormalities are profound enough to substantially increase mortality.
 Septic shock clinical criteria: Sepsis and (despite adequate volume resuscitation)
both of:
o Persistent hypotension requiring vasopressors to maintain MAP greater
than or equal to 65 mm Hg, and
o Lactate greater than or equal to 2 mmol/L
 With these criterias, hospital mortality is in excess of 40%

Sepsis is the result of a complex and dysregulated homeostatic response to infection.

Untreated sepsis progresses to hypoperfusion, hypoxia, and dysfunction at the level of
cells, tissues, and organ systems, leading to death in at least 30% of cases. The clinical
syndrome of sepsis is a manifestation of pro- and anti-inflammatory intermediates and
is intimately linked to disruptions in coagulation, microcirculatory flow, and
mitochondrial function, leading to common pathways of failure in multiple organ
systems. The severity of the response depends on both host and pathogen
characteristics and the relevant underlying pathophysiology arises principally from
interactions between an infectious agent and the host’s innate immune system.

The outcome in sepsis improves with:

1. Prompt diagnosis and treatment of the underlying cause.
2. Rapid resuscitation to prevent prolonged tissue hypoxia.
3. Good glycaemic control.
4. Strict infection control.
5. Recognition and appropriate treatment of secondary infections.
6. Adequate nutrition.
7. Recognition that ‘normal’ physiological/biochemical levels do not necessarily
need to be attained while the patient is critically ill, provided he/she is not
compromised. For example, a mean BP of 55–60mmHg is often acceptable unless
evidence of poor perfusion or ischaemia suggests higher levels should be sought.
8. Avoidance of preventable mishaps, e.g. prolonged hypotension, pressure sores,
thromboembolism.
9. Temperature control in the range 36–38.5C.
Below shows the summary of the key Surviving Sepsis Campaign guidelines
recommendations for early infection control and haemodynamic resuscitation in
patients with severe sepsis or septic shock.
In my patient, Encik Harun, his SOFA score on the second day of admission to ICU was
12. On the third day his SOFA score increased from 12 to 14. It further increased to 15
and became 17 on the fourth day despite being on IV antibiotics and triple inotropes.
REFLECTION ON ETHICS

The purpose of medicine is to preserve life and restore health, which approximately
means to cure illness and disease. When it is not possible to cure, relieve suffering and
limit disability shall then be the focus of care. Harm should be prevented. The purpose
of medicine is not to prolong life.

Maintenance of good physical and mental health is paramount as no one is capable of

performing his physical ibadat properly if one is physically and mentally handicapped.
Such effort meets the first objective of Law, which is the preservation of religion. A
healthy person is able to perform his obligation to Allah. In Islam, every good act done
with good intention, niyyah, that is for the sake Allah is considered I’badah.

The second most important goal of shariah is protection of life, coming second after the
protection of religion, which is also the ultimate aim of medicine. In Islamic teaching, life
is sacred and its sanctity guaranteed by the Holy Quran. Every life is important so
destroying life is condemned. Destroying the life of one person is equivalent to
destroying the life of all humans.

To save a person’s life by CPR or any other method is a very important necessity, as to
save one’s life it is as if one has saved the entire humanity. Like this verse mentioned in
the Holy Qur’an:

”  ‫م ْيعًا‬
ِ ‫ج‬
َ ‫اس‬ ْ َ‫ما أ‬
َ ‫حيَا ال َّن‬ َ َّ‫كأَن‬
َ ‫ها َف‬ ْ َ‫ن أ‬
َ ‫حيَا‬ ْ ‫ َو َم‬  “
Translation: “And whoever saves the life of a single person, is as if he had saved the life
of all mankind…”
Surah Al-Maidah, Verse 32

REFERENCE

1. Essential Anaesthesiology for Healthcare Professionals, 2nd Edition.

2. Oxford Handbook of Critical Care
3. The Holy Qur’an