Tetanus in The Intensive Care Unit

Tetanus in
The Intensive Care Unit

A Case Report
Lila Tri Harjana
Philia Setiawan, dr., SpAnK.IC
Departement of Anesthesiology and Reanimation

Faculty of Medicine Airlangga University
Dr.Soetomo Teaching Hospital
1
Introduction
 Tetanus is one of the ancient diseases which still
remains an enigma
 Tetanus was first described in Egypt over 3000 years
ago and was evident throughout the ancient world
 In the year 1884, Nicolaier produced tetanus in
animals by injecting them with soil specimens
 The global incidence of tetanus is about 18 cases per
100,000 population per year, with case fatality ranging
between 20 and 50%
 In 1992, out of 1000.000 patients with tetanus, over
70% died
2
Introduction…(2)
In Indonesia, Incident in Neonates is very
high, about 6-7 cases in every 1000 birth in
urban area and 11-23 cases in rural area
The treatment of tetanus in the ICU
decreased the percentage of deaths from 44
to 15, however, the cost of therapy is
considerable (estimated 1500-2500 USD a
day, with average time of the ICU
hospitalization ranging between 3 and 5
weeks)
3
Introduction…(3)
Immunization is the best and cheapest
method of preventing Death
Initial vaccination consists of three
injections performed at intervals 4-8
weeks
Immunity is established only with the
second injection, and the third prolongs its
duration
Boosters are needed at 10-yearly intervals
4
5
Pathogen
Tetanus is caused by Clostridum tetani, which is
an obligate anaerobic, gram-positive rod that is
motile and readily forms endospores
The organism is widely distributed in soil and in
intestine of horses, sheep, cattle, dogs, cats, rats,
chickens and nearly 10% of humans.
The vegetative forms are sensitive to heat and
oxygen
The spores are especially resistant to heat, usual
antiseptics and chemical agents but are destroyed
by autoclaving at 1200 C for 15 minutes or boiling
for at least 4 hours
6
7
Pathogen…(2)
 The vegetative form produces
◦ Tetanospasmin
a potent neurotoxin which is responsible for the clinical
manifestations
◦ Tetanolysin
Caused hemolytic in vitro. Its capable of damaging viable
tissue surrounding the wound and lowering the redox
potential, thus optimizing conditions for bacterial
multiplication
 Incubation period of the disease is about 7-10 days,
however, it is not impossible for the symptoms to
occur between 1 and 60 days after the injury
 The quicker the symptoms occur, the more severe
prognosis of the disease
8
Pathogen…(2)
Tetanospasmin has three predominant effects:
a) Central motor effect, where it inhibits the release of glycine (at
the spinal level) and gamma amino butyric acid (at the brain
stem) from inhibitory neurones, causing motor neurons to
respond to stimulation with sustained activity causing sustained
skeletal muscle contractions and rigidity
b) Autonomic nervous system effect, causing a loss of inhibitory
control by the spinal cord sympathetic tracts on the adrenal
medulla, leading to adrenal sympathomimetic hypersecretion.
The parasympathetic nervous system may also be affected.
c) Neuromuscular junction (NMJ) effect, causing a defect in
presynaptic release of acetylcholine, with the junction being
permanently affected and requiring the motor neurone to develop
new synapses to recover
9
Pathogenesis
 The circulating toxin does not enter the CNS directly as it cannot
cross blood-brain barrier
 The toxin binds to the gangliosides on the membranes of nerve
terminals and is then internalized and transported intra-axonally
in a retrograde direction to the cell body at rate of 75-250 mm a
day
 The toxin’s transport in the motor nerves takes 2-14 days to reach
the CNS
 Neuronal binding of the toxin is thought to be irreversible and
recovery requires the new growth of the nerve terminals, which
explains the long duration of the disease
 A postulate causes of Sympathetic Over Activity (SOA) are the
increased release of thyroid hormone and direct inhibition of the
release of endogenous opiates
10
11
Clinical Manifestation
The degree of severity varies with the
load of toxin produced at the wound site
First symptom is due to rigidity of muscle
supplied by cranial nerves, trismus being
the commonest presentation, followed by
risus sardonicus and neck stiffness
12
13
14
Philip Score
15
16
17
18
Management
Though the pathophysiology of the
disease has been explored to a molecular
level, no specific drug has been
discovered which can counteract the toxin
once it is bond to nervous tissue and the
disease established
Specific treatment is eradication of the
organism from the wound and
neutralization of the circulating toxin
19
20
21
Management…(2)
Neutralization of circulating toxin
Even if parenteral antitoxin is given as
soon as the diagnosis is made, it can only
neutralize the residual circulating toxin
IM Human Tetanus Immunoglobulin
(HTIg) is the antitoxin of choice.
The optimum does is still debatable but
500 units are recommended, as the
traditional larger doses of 3000-6000 units
are of questionable benefit
22
Management…(3)
Neutralization of circulating toxin
Equine tetanus antitoxin (ATS) is still used
in many countries (in dose of 5000 units im
and 5000 units infiltrated around the
wound) due to the nonavailability of HTIg
Parenteral antitoxin is recommended and
should be administered as soon as tetanus is
diagnosed before wound debridement, to
counteract any toxin released during the
procedure
23
Management…(4)
Eradication of the organism
Eradication of the organism is effected by
antibiotics and wide wound debridement
whenever an injury is identified
Though it has been stated that wound
debridement is of no value after the
disease has been established and that
antibiotics are of no value after wound
debridement, It may be preferable to
ensure that no further toxin is
manufactured at wound level
24
Management…(5)
Antibiotics
 Penicillin, which is effective against most clostridial
infections, was the traditional antibiotic for tetanus
 It is no longer recommended as it is GABA
antagonist and can aggravate the spasms of tetanus
 Metronidazole is preferred as it is rapidly
bactericidal against the whole spectrum of obligate
anaerobes and its pharmacokinetic attributes ensure
its distribution at effective therapeutic
concentrations even to anaerobic tissue
 Metronidazole is given in a dose of 500 mg iv every
8h for 7-10 days
25
Management…(6)
Prediction of severity
Severity should be predicted before the
onset of spasms to protect the airway
The most common method relies on the
incubation period, which is the time from
the injury to the first symptom, and onset
time, which is the period from the first
symptom to the first spasm
Prediction of severity is not fool-proof
26
Management…(7)
Symptomatic treatment
The key to symptomatic treatment consist
of controlling rigidity, spasms and
autonomic dysfunction while providing
adequate ventilation, oxygenation and
nutrition, and preventing complications
27
Management…(8)
Symptomatic treatment : Control of Rigidity & spasms
Heavy sedation, almost reaching
anesthetic levels, controls the less severe
spasms but not the rigidity
Artificial ventilation is required due to
reduced chest compliance
Drugs suppressing central or peripheral
nervous activity have been used both
separately and in combination for the
control of spasms
28
Management…(9)
Control of Rigidity & spasms : Sedatives
 Benzodiazapines and barbiturates are GABA agonist and
have gained a traditional place as sedatives for tetanus,
being inexpensive in the long-term
 Phenobarbital up to 240 mg every 8 h and amylobarbital up
to 600 mg over 24 h
 Diazepam is the more popular drug and IV doses of 15-100
mg/h are used, while doses as high as 3400 mg/day have
been reported
 Major disadvantages of diazepam are tendency to venous
thrombosis, tolerance, withdrawal symptoms (aggressive
behavior and noncooperation) and prolonged residual
sedation due to active metabolites with long half-lives (96
h)
29
Management…(10)
Control of Rigidity & spasms : Sedatives
Propofol has been successfully used in
severe tetanus according to case reports
and does not seem to be associated with
tolerance, addiction or withdrawal
symptoms
An infusion of 3,5 - 4,5 mg/kg/h
following a loading dose of 50 mg
obviates the need for other sedatives
30
Management…(11)
Supportive intensive care treatment
Infective complication of prolonged
critical illness including ventilator-
associated pneumonia are common in
tetanus
Securing the airways early in the disease
and preventing aspiration and sepsis are
logical steps in minimizing this risk
31
Management…(12)
Supportive intensive care treatment : Tracheostomy
Prior to performing this procedure, the
airway should be secured and muscle
spasms controlled
Tracheostomy is best suited for patients
with ventilatory requirements in whom a
prolonged course of disease is suspected
In such situations, tracheostomy is
preferable to endotracheal intubation
because the endotracheal tube is a potent
stimulus for reflex spasms
32
Management…(13)
Supportive intensive care treatment : Nutrition
 Weight loss is universal in tetanus
 Contributing factors : inability to swallow,
autonomic induced alterations in gastrointestinal
function, increased metabolic rate from pyrexia and
muscular activity and prolonged critical illness
 Enteral nutrition is associated with a lower
incidence of complications and is cheaper than
parenteral nutrition
 Percutaneous gastrostomy may avoid the
complications associated with nasogastric tube
feeding and is easily performed on the intensive
care unit under sedation
33
Management…(14)
New options
Tetanus has been aptly described as a third world
disease, that requires first world technology to
treat
Dantrolene produces skeletal muscle relaxation by
a direct action on excitation contraction coupling,
presumably by decreasing the amount of Ca
released from the sarcoplasmic reticulum of
skeletal muscle
Baclofen is GABA agonist and possesses many
B
of the theoretical requirements of an ideal drug for
tetanus
Baclofen does not cross the blood brain barrier
and has to be administered intrathecally
34
Management…(15)
Magnesium
 The adult human body contains approximately 2000
mEq of magnesium
 1% to 2% of the body's magnesium is present in the
extra cellular fluid,
 One third of the serum magnesium is bound to
albumin, with the rest in the biologically active
ionized form
 The normal range for serum magnesium is 1.8 to 3.0
mg/dL
 A balance between gastrointestinal absorption and
renal excretion maintains magnesium homeostasis
 In the kidney, 95% of the filtered load of magnesium
is reabsorbed in the proximal tubule and loop of Henle
35
Management…(16)
Hypermagnesaemia
 Early signs of Hypermagnesaemia, including nausea,
vomiting, weakness and cutaneous flushing, usually appear
at serum levels of approximately 3 mg/dL
 As levels rise above 4 mg/dL, hyporeflexia is seen, and
deep tendon reflexes are eventually lost
 Hypotension and ECG changes (e.g., QRS widening, QT
and PR prolongation, conduction abnormalities) are seen at
serum levels of 5 to 6 mg/dL
 Levels greater than 9 mg/dL are associated with respiratory
depression, coma, and complete heart block
 Asystole, cardiac arrest, and death have been reported in
patients with serum magnesium levels of 10 to 15 mg/dL
36
Management…(17)
Hypermagnesaemia
 The first step in the management of Hypermagnesaemia is to discontinue all
exogenous magnesium
 Patients with mild symptoms and normal renal function may require only
observation
 If more prominent symptoms are present, hydration with isotonic fluids and
administration of intravenous furosemide can be used to accelerate magnesium
elimination
 Patients with severe hypermagnesemia should receive intravenous calcium
 Calcium directly antagonizes the membrane effects of Hypermagnesaemia and
reverses respiratory depression, hypotension, and cardiac dysrhythmias
 For life-threatening manifestations of Hypermagnesaemia, 100 to 200 mg of
calcium, as either 10% calcium gluconate (93 mg calcium per ampoule) or
10% calcium chloride (360 mg calcium per ampoule), is a reasonable dose
 Repeat boluses or a continuous infusion (2-4 mg/kg/hr) may be required to
sustain the effect while measures to increase magnesium elimination are
instituted
37
Management…(18)
Magnesium in tetanus
 Magnesium (Mg) therapy has the advantage of blocking both
neuromuscular transmission and Sympathetic Over Activity
(SOA)
 At the NMJ high concentrations of magnesium compete with
calcium ions for prejunctional sites and inhibit the release of
Ach
 Mg was effective in the control of spasm and rigidity without
the need for ventilatory support in 57% of patients
 Magnesium also improves cardiovascular stability by
inhibiting neuronal and adrenal catecholamine release
reducing circulating catecholamine levels and reducing
adrenergic receptor sensitivity, thus acting as an
anticonvulsant and a vasodilator
38
Management…(19)
Magnesium in tetanus
The rate of infusion of magnesium
 Loading dose 5 g bolus over 20 min
 The hourly dose required may be as high as 4-5 g/h, which is
far greater than used in eclamsia
 Some literature suggested infusion rate 1-2,5 g/h, and in
pediatric 100 mg/Kg/24 jam (increased when necessary)
 The rate of infusion of Mg should be titrated not only to the
control of spasms but also to muscle rigidity
 The rigidity should be reduced to a level acceptable to the
patient which allows swallowing of saliva, mouth care and
limb physiotherapy
 Abolition of patellar reflex is taken as the endpoint and
evidence of hypocalcemia is judged by positive Chvostek’s
and Trousseau’s signs
39
Conclusion
 Though the pathophysiology of the disease has been explored to a
molecular level, no specific drug has been discovered which can
counteract the toxin once it is bond to nervous tissue and the
disease established
 Immunization is the best and cheapest method of preventing Death
 Even in the 21st Century, treatment is essentially symptomatic and
management regimens have not significantly improved the
outcome
 Infective complication of prolonged critical illness including
ventilator-associated pneumonia are common in tetanus
 Magnesium (Mg) therapy has the advantage of blocking both
neuromuscular transmission and SOA and also effective in the
control of spasm and rigidity without the need for ventilator
support
40
Tetanus in
The Intensive Care Unit
A Case Report
Departement of Anesthesiology and Reanimation

Faculty of Medicine Airlangga University
Dr.Soetomo Teaching Hospital
41
A case report
Name : Mr. Supriyono
Sex : Male
Age : 30 years
Height/Weight : 165 cm/ 60 kg
Register : 11003247
ICU admission : 9-12-2009
Diagnose :
Generalized Tetanus + Mild Head Injury + OF
linier R. Frontal (D) + CF linier R. Frontal (S)
42
History of Illness
3 Des 2009  4 Des 2009
Px terjatuh dikamar Px tidak bisa membuka
mandi, Kepala(dahi) mulut, sulit menelan.
terbentur seng
dikamar mandi, Tangan kesemutan, kram,
pingsan (+) sulit digerakkan
 Px dibawa ke
PKM, luka
dibersihkan dan
dijahit
R/ Pemebrian ATS (-)
43
History of Illness
 5 Des 2009
12.1 0
VK Bedah IRD RSDS
TD 130/70
N 84 x/m
RR 19 x/m
t 364 C
Dx:
Tetanus Generalisata (+) COR (+) OF R. Frontal (D) + CF R.
Frontal (S) + Hematosinus Frontalis (S)
MRS di R. Tetanus Bedah G

44
Philip Score:
Masa inkubasi : 2 hari 4
Tempat infeksi: kepala 4
Imunisasi: > 10 th 4
Faktor penyerta: trauma 4
16
45
Thoraks 05-12-2009
46
47
48
Laboratory Finding
Hb 13,3 Na 164,4
Hct 38,2
K 4,08
Leu 8,9
Thro 315 Cl 134,1
GDA 86
BUN 9,0
SK 1,0
SGOT30
SGPT 28
Alb 4,2
49
Terapi di R. Tetanus Bedah G
06-12-2009 s/d 08-12-2009
Infus RD5 1500 cc/24jam
Inj PP 3 x 1,5 juta iu
Inj metronidazole 3 x 500mg
Inj Diazepam 8 amp / 24 jam (syringe pump)
Inj antrain 3 x 1 amp
Diet sonde TKTP
Oral hygiene
Mobilisasi mika miki
Rawat luka
50
R. Tetanus Bedah G
08-12-2009, pk 17.25
Kejang (+)  inj Diazepam 1 amp
diencerkan 10 cc bolus iv
Gasping  O2 masker 10lmp
TD 90/60, N 90, RR 40grojok PZ
500cc  sadar, TD 100/80, N 80, RR 24
Diazepam 8 amp/24jam  10 amp
/24jam
51
History of Illness
09 Des 2009
Px dikonsulkan ke ICU karena Airway & Breathing problem
 B1 A gargling & trismus  coba dibuka dg tongue spatel 
hipersekresi  suction  bebas
B spontan simetris 22-24 x/m ves +/+ rh +/+ wh -/-
Thorax foto: infiltrat di kedua lapang paru
 B2 P HKM TD 110/80 n 106 x/m
 B3 GCS 4X6 (trismus)
 B4 BAK terpasang kateter BGA O2 40%
 B5 Abd supel  pH 7,41
 B6 lordosis (-)  pCO2 38,2
 pO2 145
 HCO3 19,6

Konsul dr.PS, Sp.An.,KIC : ACC Masuk ICU BE -5
 SO2 99%
52
ICU Hari 0(Pk. 13.00)
B1 : A :Partial Obstruksi, Gargling, Trismus
B :Spontan RR: 24 x/m ves +/+ rh +/+ wh-/-
B2 :pHKM, CRT<2
TD: 120/70 N:110 x/m
B3 :GCS 4X6 (Trismus)
B4 :BAK terpasang Kateter
B5 : Abd soepel
B6 : Lordosis (-)
53
Thoraks 09-12-2009
54
Advis dr PS SpAnKIC
Cek Ca, Mg, BUN/SK sebelum MgSO4
diberikan
Bolus MgSO4 1g, dilanjutkan
maintanance MgSO4 100mg/Kg/24 jam
Evaluasi Reflek Patella tiap jam dan Prod
Urin tiap 3 jam
Cek Mg, Ca tiap 6 jam
55
ICU Hari 0
Initial Therapy:
 O2 Masker Reservoar
 Stable side position
 Fisioterapi nafas + nebul ventolin 6x/hr
 Oral + personal hygiene
 Sonde PE 6 x 100 cc
 Inf. RD5 2000 cc/24 jam
 Inj. PP 3 x 1,5 jt unit im (5)
 Drip metronidazole 3 x 500 mg iv (5)
 Inj. Antrain 3 x 1 g iv
 Inj. Ranitidine 2 x 50 mg iv
 Bolus MgSO4 1000mg (MgSO4 20% 5 cc)  maintanance
100mg/Kg/24 jam (MgSO4 20% 30 cc / 24 jam)
56
ICU
Keluarga ingin PP di KIE ulang minta waktu
untuk berunding (pemeriksaan Ca,Mg belum
bisa dikerjakan)
Kondisi pasien
A: Trismus, hipersekresi ↑↑
B: Spontan RR: 28-32x/m, Flare +/+, SN
ves +/+, Rh +/+, wh -/- sat O2: 90 % 
dgn O2 masker reservoir
C: pHKM, CRT<2
TD: 128/84 , N:132x/m
57
ICU
Intubasi
Induksi : Midazolam 4 mg +
atracurium 30 mg
ETT Ø 7.5 Cuff(+), Sim +/+, Fiksasi
+/+
58
ICU
Pk. 18.00 c.dr.PS, Sp.An.,KIC :
Puasa dulu sampai besok, cairan min. 2000 cc
Ranitidine inj. 2x1 amp.
Cek refleks patella  bila (-)  cek Ca, Mg
tiap 3 jam
Bila kejang (-) cukup MgSo4 saja
Pk. 00.00 Konsul dr.PS, Sp.An.,KIC :

Refleks patella menurun  MgSO4 75
mg/kgB/hari
59
Laboratory Finding
(Pk. 17.30) (17.30)

BUN16,0 BGA O2 masker
pH 7,44
SK 1,5 pCO2 37
Ca pO2 169
10,0 HCO3 24,4
Mg BE 0,6
(Pk. 23.30) 2,4
SO2 99%
Ca 10,1
Mg 2,5
60
Observasi Vital Sign ICU Hari 0
09-12-2009
Rflk Patela (-)
Intubasi
MgSO4 75 mg/Kg/hari
MgSO4 100mg/Kg/hari
61
Pemberian MgSO4 Hari 0
09-12-2009
62
ICU Hari 0
Therapy:
O2 Ventilator
(Posisi slight head up)
Fisioterapi nafas + nebul ventolin 6x/hr
Oral + personal hygiene
Sonde PE 6 x 100 cc
Inf. RD5 2000 cc/24 jam
Inj. PP 3 x 1,5 jt unit im
Drip metronidazole 3 x 500 mg iv (6)
Inj. Antrain 3 x 1 g iv
Inj. Ranitidine 2 x 50 mg iv
MgSO4 sp 75 mg/kg/24 jam  0,9 cc/jam
63
ICU Hari 1 10 Desember 2009
 B1 : A :Bebas Tube-in
B :Ventilator mode BIPAP ASB 6, PEEP 8, Pinsp 16, f 8 , FiO2
30%
 Vt 470-564, f13-14, MV 7.57-8.14, SpO2 98-100%
 B2 :pHKM, CRT<2, Cor : dbn
TD:120/70 N: 103x/m
 B3 :GCS 4X6 (Intubasi)
 B4 :BAK terpasang Kateter
B5 : Abd soepel
 B6 : Lordosis (-)
64
Thoraks 10-12-2009 (post Intubasi)
65
Laboratorium 10 Desember 2009
BGA (BIPAP ASB 6, PEEP 8, Pinsp 16, f 8 , FiO2 30%
 Vt 470-564, f13-14, MV 7.57-8.14, SpO2 98-100%)
pH 7,41
pCO2 31 •Hb 12,7
pO2 145 •HCT 36,6
HCO319,6 •Leko 19,8
BE -5 •Trombo 303
SO2 99%
•Na 149,1
Bun/SK
•K 3,65
15/0,9 •Cl 110,4
SGPT 55
66
10-12-2009
67
10-12-2009
68
ICU Hari 1
Therapy:
 O2 Ventilator
(Posisi slight head up)
 Sonde PE 6 x 100 cc  cek retensi
 Inf. Pan Amin G 500 cc + KaEnMG3 1500 cc/24 jam
 Inj. Antrain 3 x 1 g iv
 MgSO4 sp 75 mg/kg/24 jam  100 mg/kg/24jam
 Paracetamol 4 x 500mg bila Temp>38 0C
69
B :Ventilator BIPAP ASB 6 Vt 470-564
PEEP 8 f 13-14
Pinsp 16 MV 7.57-8.14
f 8 SpO2 98-100%
FiO2 30%
Tinsp 1.4
TD:110/63 N: 80-100x/m
 B5 : Abd soepel
 B6 : Lordosis (-)
70
11-12-2009
71
11-12-2009
72
ICU Hari 2
Therapy:
 O2 Ventilator
 Posisi slight head up
 Sonde PE C1-C3 3 x 200 cc  cek retensi
C4-C6 3 x 250 cc  cek retensi
 Inf. KaEnMG3 1500 cc/24 jam
 Sucralfat 3 x C I personde
 OMZ 3 x 1
 MgSO4 sp 75 mg/kg/24 jam  100 mg/kg/24jam
73
B :Ventilator CPAP ASB 6, PEEP 8 , O2 30%
 F 19, MV 8-9, TV 350-450
TD:116/67 N: 98-99x/m
 B5 : Abd soepel
 B6 : dbN
74
12-12-2009
75
12-12-2009
76
PPT13,8/11,9
APTT 30,3/25,5
Na 147
K 3,7
77
ICU Hari 3
Therapy:
 O2 Ventilator
 OMZ 3 x 1  stop
 MgSO4 sp 100 mg/kg/24jam
78
B :SR 18-20 x/mnt, SN Ves+/+, Rh-/-, Wh-/-
TD:127/84 N: 86-90x/m
 B5 : Abd soepel
 B6 : dbN
79
13-12-2009
80
13-12-2009
81
ICU Hari 4
Therapy:
 O2 Ventilator
82
B :SR 20 x/mnt, SN Ves+/+, Rh-/-, Wh-/-
TD:120/70 N: 90-110x/m
 B5 : Abd soepel
 B6 : dbN
83
14-12-2009
84
14-12-2009
85
ICU Hari 5
Therapy:
 O2 Ventilator
86
dg O2 T piece  SpO2 99-100%
TD:124/68 N: 90-100x/m
 B5 : Abd soepel
 B6 : dbN
87
15-12-2009
88
15-12-2009
89
ICU Hari 6
Therapy:
 O2 T Piece
 Jus Buah 1 x 200 cc
 As Mefenamat 3 x 500 mg personde
90
 B1 : A :Bebas Tube-in  Tracheostomy
dg O2 T piece  SpO2 99-100%
TD:114/65 N: 100x/m
 B3 :GCS 4X6
 B5 : Abd soepel
 B6 : dbN
91
16-12-2009
T
R
A
C
H
E
O
S
T
O
M
Y
92
16-12-2009
93
Hb 12,4
HCT 39,1
Leko14,9
Trombo 589
Hasil Kultur 10-12-09 s/d 16-12-09

Darah : steril
Urin : Steril
Dahak : Steril
94
ICU Hari 7
Therapy:
 O2 T Piece via tracheostomy
95
 B1 : A :Bebas Tracheostomy
dg O2 masker via tracheostomy  SpO2 100%
TD:124/68 N: 90-100x/m
 B3 :GCS 4X6 (Tracheostomy)
 B5 : Abd soepel
 B6 : dbN
96
17-12-2009
97
17-12-2009
98
ICU Hari 8
Therapy:
 O2 T Piece via tracheostomy
 Rawat Traceheostomy
 Inf. Kalbamin 500 cc/24 jam
99
TD:120/75 N: 100x/m
 B5 : Abd soepel
 B6 : dbN
100
18-12-2009
101
18-12-2009
102
ICU Hari 9
Therapy:
 O2 masker via tracheostomy
 Mobilisasi mika-miki
 Inf. KaEnMg3 500 cc/24 jam
 Dulcolax 2 tab malam
103
TD:115/60 N: 90-100x/m
 B5 : Abd soepel
 B6 : dbN
104
19-12-2009
105
19-12-2009
106
ICU Hari 10
Therapy:
 Inj. PP 3 x 1,5 jt unit im (15)  stop
107
TD:125/80 N: 100x/m
 B5 : Abd soepel
 B6 : dbN
108
20-12-2009
109
20-12-2009
110
ICU Hari 11
Therapy:
111
TD:124/80 N: 100-110x/m
 B5 : Abd soepel
 B6 : dbN
112
21-12-2009
113
21-12-2009
114
ICU Hari 12
Therapy:
 Sucralfat 3 x C I personde  stop
 Inj PP 3 x 1,5 juta iu iv (16)
 Dulcolax 2 tab malam
115
TD:125/60 N: 90-100x/m
 B5 : Abd soepel
 B6 : dbN
116
22-12-2009
117
22-12-2009
118
ICU Hari 13
Therapy:
 Inj PP 3 x 1,5 juta iu iv (17)
 Dulcolax 2 tab malam 119
Vital Sign selama 13 hari di ICU
120
Pemberian MgSO4 Selama 13 hari
121
Pembahasan
• Pemberian Diazepam dengan dosis 100 mg/24 jam masih
jauh dari dosis rekomendasi untuk terapi tetanus
• Pemberian MgSO4 memerlukan observasi yang ketat,
mengingat rentang dosis terapi dan toksik yang sangat
sempit
• Loading dose 5 gram bolus selama 20 menit untuk mecapai
therapeutic plasma level
• Dosis maintanance dapat dinaikkan mencapai 5 g/jam
selama monitoring intoksikasi dapat dilakukan dengan baik
• Pemberian magnesium pada pasien ini memberikan
dampak penurunan secara klinis dari spasme dan rigiditas
yang terjadi
122
Pembahasan
• Pemberian Antibiotik Peniciline secara teori dapat
menimbulkan spasme oleh karena peniciline adalah GABA
antagonis
• Metronidazole adalah antibiotik yang dianjurkan dengan lama
pemberian 7-10 hari
• Pemberian nutrisi harus menjadi perhatian penting pada
perawatan pasien dengan tetanus
• Selama tidak ada komplikasi GI tract, Nutrisi enteral dapat
diberikan dengan tetap waspada terhadap bahaya aspirasi
• Perawatan penderita tetanus di ICU secara umum sama dengan
perawatan pasien dengan critical ill yang lain dengan tetap
memperhatikan kemungkinan komplikasi selama perawatan
diluar komplikasi yang disebabkan tetanus
123
Pembahasan
Penanganan tetanus setelah eradikasi
kuman dan eliminasi circulating toksin
adalah supportive
Penyembuhan dari tetanus membutuhkan
waktu minimal 3-6 minggu untuk
memberikan kesempatan regenerasi
neuron yang terikat dengan toksin tetanus
124
Terima Kasih
125

Tetanus in The Intensive Care Unit

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Tetanus in The Intensive Care Unit

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Tetanus in

The Intensive Care Unit

Lila Tri Harjana

Philia Setiawan, dr., SpAnK.IC

Departement of Anesthesiology and Reanimation

Departement of Anesthesiology and Reanimation

MRS di R. Tetanus Bedah G

Pk. 00.00 Konsul dr.PS, Sp.An.,KIC :

(Pk. 17.30) (17.30)

Hasil Kultur 10-12-09 s/d 16-12-09

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