Emergency department assessment and management of Quadriparesis in ER

1. APPROACH AND MANAGEMENT OF ACUTE ONSET
QUADRIPARESIS/QUADRIPLEGIA IN
EMERGENCY DEPARTMENT Approach and
management of acute onset quadriplegia in emergency
department
Dr G . Vishwa Reddy
Department of Emergency Medicine
Nizam’s Institute of Medical Sciences

2. Introduction
• Quadriplegia or Quadriparesis refers to the partial or complete paralysis of all
four extremities as well as the torso. It may be flaccid or spastic.
• The loss is usually sensory and motor, which means that both sensation and
control are lost.
• Quadriplegia/Tetraplegia is caused by damage to the brain or the spinal cord at a
high-level C1–C7 ,in particular, spinal cord injuries secondary to an injury /
damage caused by systemic illness , local lesion or damage to the cervical spine
.

3. Clinical presentation
• Loss of movement
• Loss of sensation, pain ,tingling and numbness
• Loss of bowel or bladder control
• Exaggerated reflex activities or spasms
• Difficulty breathing ,coughing or clearing secretions from the lungs
• Changes in the sexual function ,sensitivity and fertility

4. American Spinal Injury Association Impairment Scale
• A - Complete - No motor or sensory function is preserved in the sacral segments S4–S5.
• B - Incomplete - Sensory function preserved but not motor function is preserved below
the neurological level and includes the sacral segments S4–S5.
• C - Incomplete -Motor function is preserved below the neurological level; more than half
of key muscles below the neurological level have a muscle grade less than 3.
• D - Incomplete - Motor function is preserved below the neurological level; at least half of
key muscles below the neurological level have a muscle grade of 3 or more.

5. Case -1
Chief complaint: 72 yr / M c/c progressive weakness in all four limbs since one week ,
tingling numbness in one week
H/o Present illness: gradual in onset rapidly progressive weakness , h/o fever present , no
h/o cough ,sore throat , headache , vomitings , seizures , involuntary bowel and bladder
movements , no h/0 trauma .
Primary Survey :
Airway : Patent , Breathing –RR - 14 , Spo2- 95 % RA , Circulation : Pulse -90 , BP- 130/80 ,
Disability -GCS - 15/15.
Secondary Survey :
General examination : moderately built and nourished , P( + ), I ,C ,K, L , E( - ve )
Systemic examination : CNS : HMF - Normal ,Cranial nerves - WNL , Motor - (Tone-
increased , Bulk –WNL )

6. Power Rt – 2/5UL , 4/5 LL , Lft- 3/5 UL , 4/5 LL) ,Reflexes- UL 2 + , LL 3 +
Plantars – Biltrl extensor , Sensory - WNL , Bowel Bladder involvement- No ,
Cerebellar signs and Gait – could not be assessed .
Meningeal signs – absent
Investigations : ABG , Serum electrolytes , CBP , CT Cervical and Dorso lumbar spine .
Provisional Diagnosis : ? GB syndrome , CVA , R/o Potts Spine , SOL .
Case -1

7. Case -2
Chief complaint: 30yr/M c/c – weakness of the upper limbs and lower limbs-10 days ,
vomitings -3 episodes since 1 day ,shortness of breath -2 days ,
H/o Present illness: h/o of inability to walk + , no h/o of loss of sensation in the limbs ,
deviation of mouth + ,
no h/o fever , altered sensorium, trauma , headache , blurring of vision ,back pain, no h/o
loose motions ,abdomen pain , no h/o of chest pain, palpitations , pedal edema , cough
,haemoptysis .
Primary Survey :
Airway – Patent , Breathing –RR-30 ,Spo2- 95 % RA , Circulation - Pulse -90 , BP- 80/50 ,
Disability -GCS - 15/15 , pupils –NS RL +, GRBS – 180
Secondary Survey : General examination : moderately built and nourished P(+),I ,C ,K, L,E( -ve )
Systemic examination : CNS : HMF - Normal ,Cranial nerves - WNL , Motor –
( Tone- decreased biltrl, Bulk WNL), Power Rt – 3/5 UL 2/5 LL , Lft - 3/5UL 2/5 LL) ,Reflexes –
DTR absent in all four limbs , Plantars – Biltrl flexor .

8. Sensory - WNL , Bowel ,Bladder involvement - No ,
Cerebellar signs and Gait - could not be assessed ,
Systems review : CVS , RS – Biltrl AE + , Crepts + , and GIT – WNL
AMPLE H/o : Htsn ,DM , h/o similar complaints in the past , no significant allergic h/o ,
no prior intake of any medication .
Provisional Diagnosis : ? Hypokalemic paralysis , renal failure ,
K/c/o DM , Htsn , R/ o Systemic Envenomation .
Inv : ABG , ECG , Serum electrolytes , RFT , MRI Spine
CASE-2

9. Case -3
Chief complaint: 40 /M , c/c weakness of all four limbs , inability to walk since –I day
H/o Present illness: sudden onset weakness , giddiness + , no h/o LOC , Seizures , vomitings ,
no h/o trauma , no h/o head ache , fever , cough , SOB , decreased urine output , incontinence of bowel
and bladder +
Primary Survey :
Airway – Patent , Breathing –RR-30 , Spo2- 91 % RA , Circulation : Pulse -90 , BP- 110/70 ,
Disability -GCS - 15/15, pupils –NS RL +, GRBS – 180
Secondary Survey :
General examination : moderately built and nourished P, I ,C ,K, L , E( - ve )
Systemic examination : CNS : HMF - Normal ,Cranial nerves - WNL ,Motor - (Tone increased in all four
limbs ,Bulk - WNL), Power Rt – O/5 UL , O/5 LL , Lft- 0/5 UL ,0/5 LL) ,Reflexes – UL -2+ , LL -3+ ,
Plantars – Biltrl extensor , Sensory - Absent below C2 , Cerebellar signs –could not be assessed,
Meningeal signs - Absent

10. Systems review : CVS , RS and GIT – WNL
AMPLE H/o : no significant past and allergic h/o , h/o administration of ASV in
a local hospital .
Provisional Diagnosis : ? CVA , Snake Bite , R/o GB Syndrome .
Inv: ABG , Serum electrolytes , CT Brain , NCS , DW MRI Brain ,
MRI spine .
Case- 3

11. Case -4
Chief complaint: 52 yr /Fe , C/c Progressive weakness of all four limbs , inability to speak since 5 days ,
and shortness of breath – 2 days
H/o Present illness : weakness associated with dysphasia + , no h/o of headache , vomitings , seizures ,
back ache , bowel bladder incontinence , h/o fever , cough , SOB +
Primary Survey :
Airway – Protected , Breathing – RR-40 , Spo2- 95 % on ventillator , Circulation : Pulse - 116 , BP- 130/70
Disability -GCS – E3 VT M4 , Pupils –NS RL +, GRBS – 116
Secondary Survey :
General examination : moderately built and nourished P( +ve), I ,C ,K, L , E( - ve )
Systemic examination :
CNS : HMF - WNL , Cranial nerves - WNL , Motor - (Tone- decreased , Llimbs < Ulimbs , Bulk - WNL),
Power Rt – 3/5 UL , 1/5 LL , Lft- 2/5 UL ,1/5 LL , Reflexes – absent , Plantars – Biltrl flexor ,
Sensory - WNL , Cerebellar signs –could not be assessed , Meningeal signs - Absent

12. Case- 4
Systems review : CVS , RS and GIT – WNL
AMPLE H/o : Past H/o – Htsn , Hypothyroid , No significant allergic h/o ,
h/o administration of IV Immunoglobulin in a local hospital .
Provisional Diagnosis : ? GB Syndrome , Systemic Envenomation , Hypokalemic
paralysis , R/o CVA - with respiratory failure on Ventillator .
Inv : ABG , Serum electrolytes , NCS , DW MRI .

13. Case -5
Chief complaint : 35 yr / M , Alleged h/o of fall from tree on 24/7/19 , followed by inability to walk and loss
of sensation in both lower limbs and abdomen below the region of umbilicus, pain and tenderness
in the chest region .
H/o Present illness : h/o vomiting + , incontinence of bladder + , no h/o of LOC , seizures , ENT bleed .
Primary Survey :
Airway – Patent , Breathing – RR- 22 , Spo2 - 97 % RA , Circulation- PR -96 , BP – 100/70 , Disability – E4V5M6
,Pupils – 2mm RL + , GRBS – 128 .
Secondary Survey :
Head – No E /0 of HI , C Spine tenderness – absent , CCT + ve , P/A – Soft , no tenderness , PCT – ve ,
Extremities – Motor -Tone : WNL , Power : UL- Rt 5/5, Lft 5/5 ,LL -Rt 1/5 Lft 2/5, Sensory - S loss
Below T12 , L1 , Reflexes - UL 1 + , LL absent , All peripheral pulses + .
Log roll : Tenderness + Thoracic and lumbar spine region , Anal tone –lost .

14. Case : 5
AMPLE H/o : No significant past , allergic and medical h/o , Exposure – No visible
injuries .
Systemic Examination : CVS , GIT – WNL , RS –Tenderness + lft side , BAE +,
No added sounds .
Provisional Diagnosis : Traumatic Paraplegia with Blunt Injury Chest.
Inv : ABG , Chest Xay , CT Brain , MRI DL Spine

15. DISCUSSION
Primary Survey : Immediate Interventions
• Ensure protection of airway and adequate ventilation
(Especially if there is respiratory muscle weakness, shallow
respiration, dysphagia, weak gag reflex)
• Check and support: BP and Heart Rate
• Immobilize neck if history of neck/head trauma
• Send electrolytes and get an ECG- to look for hypo/hyperkalemia

16. CLINICAL EXAMINATION CLUES TO DIFFERENTIAL DIAGNOSIS
• 1: Is it an upper motor neuron (UMN) or a lower motor neuron
(LMN) lesion?
• Clues to UMN lesion (mostly a spinal cord lesion) could be presence of
either:
• Brisk reflexes
• Extensor plantar
• Definite sensory level
• Bladder or bowel involvement
• A LMN lesion will have absent reflexes with mute plantar.
• Frequently, an acute onset spinal cord lesion may present with
absent reflexes due to spinal shock. But the presence of other
differentiating features (extensor plantar, definite sensory level
and bladder involvement) help to localize the lesion to spinal cord.

17. • Step 2: If it is a LMN lesion what is the pattern of weakness?
• Is it proximal or distal?
• Lesions localized to the following anatomical locations cause proximal, mostly symmetrical weakness in
AFP: • Muscle • NMJ • Polyradiculoneuropathies
Poly neuropathy will present with distal, mostly symmetrical weakness.
Lesions localized to the anterior horn cells can present with symmetrical or asymmetrical, proximal, distal
or a combination of both. The reflexes will be absent in both the conditions.
Step 3: Are the reflexes preserved?
Localization of lesions with proximal weakness and preserved reflexes include muscle or NMJ. Fatigability
(appearance of weakness with repeated use) is a prominent feature in NMJ disorders especially myasthenia.
Reflexes would be absent in: • Anterior horn cell disorders • Polyradiculoneuropathies • neuropathies
Step 4: Are sensations preserved?
Neuropathies present with sensory involvement.
Polyneuropathy presents with glove and stocking sensory involvement while mononeuritis multiplex
would present with patchy sensory loss.
Polyradiculoneuropathies may or may not have a sensory loss.
Some GBS variants may have sensory loss. Cauda equina may present with a sensory loss in a
radicular distribution.

18. Approach for Clinical Examination

19. Examination and classification into pattern
• Flaccid quadriparesis with sensory level (early bladder dysfunction)- Transverse myelitis,
compressive myelopathy.
• Flaccid afebrile symmetric Para/Quadriparesis (+/− bulbar and Respiratory involvement) with
areflexia and minimal sensory loss (but often sensory symptoms) : Acute neuropathy or
polyradiculopathy (esp., Guillain Barre Syndrome).
• Flaccid, febrile, pure motor, asymmetric, paralysis (no bladder involvement) often with
meningismus: Enteroviral, polio, or vaccine associated poliomyelitis.
• Ophthalmoplegia, ptosis, bulbar weakness with motor weakness: Guillain Barre Syndrome,
Botulism, Myasthenia Gravis.
• Proximal muscle weakness, muscle tenderness without sensory symptoms or signs and with
preserved reflexes: Viral myositis, inflammatory myopathy (e.g., dermatomyositis) .

20. Investigations (according to the suspected
site of lesion /cause of paralysis)
• ECG: Hypo/Hyperkalemia
• Biochemistry:, Potassium, Magnesium, Phosphate, Creatine Kinase .
• Toxic screen: Urine for porpho-bilinogens, arsenic, lead etc.
• X- ray spine: suspected atlantoaxial dislocation, vertebral tuberculosis.
• Neuroimaging (spinal cord) MRI indicated in all cases of myelopathy, suspected
transverse myelitis.
• Electrophysiological testing (NCV & electromyography/ RNST): Guillain Barre Syndrome,
Myasthenic Crisis, Inflammatory Myopathy, Periodic Paralysis (Dyskalemic), acute
neuromyositis.
• Lumbar puncture (CSF): Guillain Barre syndrome, suspicion of viral myelitis

21. Provisional Diagnosis
• Clinical Diagnosis –What is the
probable lesion.
• Anatomical Diagnosis- Where is the
lesion.
• Pathological Diagnosis- How is the
lesion caused .

22. DIFFERENTIAL DIAGNOSIS
The initial E D differential diagnosis with or
without alteration of sensorium , bowel and
bladder involvement include :
1.Systemic Envenomation : Snake Bite , Botulism
,Tick Paralysis , Heavy metal poisoning , Alchoholic
intoxication , Scorpion sting.
2. Guillian Barre syndrome
3.Electrolyte disturbances :
Hypokalemia , Hyperkalemia , Hypercalcemia ,
Hyper - Hyponatremia , Hypermagnesemia and
Hypophosphatemia.
4. Central Nervous system disorders :
Transverse
Myelitis , Multiple Sclerosis, Ischemic , Vasculitic ,
tumours , traumatic cord lesions.
5. Disorders of neuromuscular junction :
Myasthenia gravis , Lambert Eaton syndrome .
6.Muscle disorders : Myopathies and
channelopathies .
7.Infectious causes : Bacterial
osteomyelitis ,Spinal abcess ,
Poliomyelitis Diphtheria, Dengue
fever HIV, Lyme disease.
8.Vascular causes : Anterior spinal
artery occlusion , AV malformation .
9. Vertebral Disease : Vertebral disc
prolapse , Pagets disease ,Spinal
deformity, Spondylosis .
10 .Others : Degenerative Motor Neuron
disease , Decompression Syndrome,
Metastasis, Hereditary spastic paresis,
Epidural , Intramedullary haemorrhage .

23. Review of Cases– Case 1

24. Review of Cases- Case 2

25. Review of cases – Case 3

26. Review of Cases – Case 4
GB Syndrome – Acute motor
axonal neuropathy
(AMAN – variant)
Diagnosis NCS studies
• When GBS is suspected ,electro-physiologic studies
are essential to confirm the diagnosis and exclude its
mimics.
• The differentials of pure motor syndrome includes
other diseases such as myasthenic crisis ,acute
presentation of idiopathic inflammatory myopathies
,and the unusual motor neuron disease patients
presenting with acute respiratory failure.
• The finding of multifocal demyelination on early
electro diagnostic testing , (or repeated a week later)
is extremely helpful in confirming the diagnosis of
AIDP , with high sensitivity and specificity .

27. Review of Cases – Case 5

28. ED Treatment and Disposition
( )
Anticipate , Identify and Treat
1. Meticulous Supportive care - Respiratory, bulbar weakness , Spinal Immobilization- if required
Shock due to reduced vascular tone (spinal cord disease) , autonomic instability .
2. Specific therapy: ( Initiated In -Consultation with Primary department )
• Hypokalaemia: Intravenous potassium correction
• Guillain Barre syndrome: IVIG, 2 g/kg over 2–5 d
• Transverse myelitis: IV methyl-prednisolone 10–30 mg/kg, daily (max-1 g) for 3–5 d
• Compressive myelopathy& Acute traumatic : Spinal immobilization, steroids ,
Spinal cord injury Neurosurgical intervention .
• Dermatomyositis, Myasthenia Gravis: Immunomodulation
3. Prevention of nosocomial infections and complications of immobilization .

29. Algorithm for ED Management of Quadriparesis/plegia

30. Evidence Based Teaching / Key Points
• Quadriparesis represents a diagnostic challenge because of its
multidimensional etiology: neurological, metabolic, endocrinal,
and biochemical factors.
• A protocol based clinical and investigational approach accompanied by
aggressive treatment stratergies , if initiated would preserve neurologic
function and prevent complications.

31. THANK YOU !!