Post-Stroke Dysphagia: Incidence, Diagnosis and Complications

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1 Original Article Post-Stroke Dysphagia: Incidence, Diagnosis and Complications Wafik M. El-Sheikh Department of Neuropsychiatry, Minoufiya University; Egypt ABSTRACT Background: Swallowing dysfunction can complicate acute stroke and directly affect patient's prognosis and recovery through development of chest infection (respiratory morbidity), nutritional problems and dehydration. Objective: To study the relationship of post stroke dysphagia (assessed clinically and by pulse oximetry) with the stroke 'site and size, and with subsequent in hospital respiratory morbidity and mortality. Also to determine the predictive value of both tests, for respiratory morbidity Methods: Forty patients with acute stroke were examined neurologically. Staff Swallowing Assessment (SSA) was performed within hours of admission along with pulse oximetry. Strokes were classified according to brain CT or MRI. In hospital respiratory morbidity and mortality, mode of nutrition and disability status at discharge were recorded. Results: Eighteen patients (%) developed post stroke dysphagia (unsafe swallowing) during their hospital course, but only thirteen patients (.%) developed respiratory morbidity. In the hemorrhagic group % developed dysphagia and chest infection, but only 9% of the ischemic group developed dysphagia and % developed chest infection. Dysphagia was more common among those who had large seized lesion or GCS<1 or brain stem lesion. SSA had a sensitivity and specifity % and % respectively for predicting respiratory morbidity. Pulse oximetry corresponding figures were % and 9%. Conclusions: The presence of large sized lesion or GCS<1 is significantly related with subsequent dysphagia, respiratory morbidity and mortality. SSA failure and desaturation >% on pulse oximetry are also significantly related with dysphagia, respiratory morbidity and mortality and dependency status at discharge. (Egypt J Neurol Psychiat Neurosurg. 1; (1): 1-1) Key Words: acute stroke, dysphagia, respiratory morbidity. INTRODUCTION Dysphagia is a common morbidity after stroke, but its frequency is widely distributed between 19-1% 1, and it is associated with increased risk for pulmonary complications and even mortality 1,. Early detection of dysphagia reduces these complications and also the length of hospital stay and overall cost,. Dysphagia was earlier hypothesized to result only with bi- cortical involvement or brainstem affection -. However, it is now proven that unilateral hemisphere or brain stem strokes can also cause dysphagia 9-1. Dysphagia complicates the course of acute strokes through its potential of development of chest infection, nutritional problems and dehydration 1,1. Patients with dysphagia are more likely to require care in rehabilitation centers. 1 Dysphagia is also an independent predictor of respiratory morbidity and mortality in acute stroke 1,19. In this prospective study, the aim was to study the relationship of dysphagia following stroke with the type, site and size of stroke. Correspondence to Wafik M. El-Sheikh, Department of neurology, Minoufiya University, Egypt. dr.wafeek@yahoo.com Tel: + 19 The aim was also to determine morbidity and mortality in patients having dysphagia following stroke and to determine the predictive value of individual parameters in the Standardized Swallowing Assessment {SSA} and the pulse oximetry 1 for prediction of chest infection. PATIENTS AND METHODS The study was carried out in El-Rehab private hospital in Tanta city, Egypt from January to October. Forty patients, admitted within h of acute stroke (infarction or bleeding) were serially taken. Exclusion criteria: Patients presenting after h of stroke onset, patients with Glasgow coma score (GCS) less than 1, and patients who were unable to sit up for SSA, or those who have chronic obstructive lung disease; or severe peripheral vascular diseases that could affect pulse oximetry' results. Detailed history, standard clinical neurological examination and brain CT or MRI were done for each patient. Patients were classified according to type of stroke and lesion site and size. Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1 1

2 Standard Swallowing assessment (SSA), (a bedside test consists of stages, used for assessing dysphagia was carried out in all patients within h of admission. Pulse oximetry using (EAGLE monitor M FF9G, series 1 Respiration, MarQuette Electronics, WILW WI USA) was performed simultaneously with different stages of SSA. Patients with desaturation % from his baseline were judged as aspirator. All patients were monitored daily for development of chest infection. The parameters checked were tachypnoea (RR>/min), tachycardia, fever, inspiratory crackles / bronchial breathing, X-ray evidence and hypoxia on arterial blood gases (ABG). Presences of three or more findings were taken as indicators of chest infection. 1 The mode of nutrition during hospital stay and at discharge [Intravenous (IV), Ryle's tube (RT), oral] was noted. The final outcome was studied in terms of recovery from chest infection and dysphagia and neurological recovery. Patients with residual neurological deficit and dysphagia at discharge were labeled as having partial recovery with nasogastric tube dependence. Those with only neurological deficit and no dysphagia at discharge were labeled as having partial recovery. Statistical analysis Results were collected, tabulated and statistically analyzed by IBM personal computer and statistical packages SPSS V. 1. The Chi-Square test was utilized for finding the relationship between the results. The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of each SSA parameter for predicting respiratory morbidity was assessed with x tables. The sensitivity and specificity of SSA in its entirety and pulse oximetry for assessing dysphagia was calculated as per standard formulae. RESULTS Forty patients (F, 1M with mean age.. years) included in this study; of them had cerebral infarction and had c.hemorrhage. Eighteen patients (%) developed dysphagia and thirteen patients (.%) developed chest infection. Laterality has no significant (P>.) effect on development of dysphagia and chest infection [Table 1]. Five out of seven (%) patients with c.hge. developed unsafe swallowing, which is significantly (P<.) more common than safe swallowing among this group and also significantly more common than ischemic group (9%). But safe swallowing was significantly more common (P<.) than unsafe swallowing among patients with sub-cortical infarction (%) than cortical (%) or brain stem (%) infarction [Table 1]. Regarding the volume of the lesions, all patients (1%) of those having large lesion developed dysphagia, % of them developed respiratory morbidity, this is highly significant (P<.1) in comparison to those with small sized lesions and also to those with medium sized lesions (P<.). All patients (1%) with GCS<1 had unsafe swallowing and respiratory morbidity which is significant (P<.) in comparison to those who had GCS>1; where only % of them had dysphagia. But safe swallowing (P<.) and healthy chest (P<.1) were significantly more common among those with >1 GCS (Table 1). The patients in the safe swallowing group () did not show any mortality and non of them had RT feeding during their course (residual dysphagia); 1 of them recovered fully and 1 patients recovered with partial neurological deficit (Table ). The following results were further obtained: Death is highly significant (P<.1) among patients with dysphagia than those with safe swallowing. Two out of seven (9%) of the hemorrhagic group were expired, while only % of the ischemic group were expired. Marked recovery recoded in 1% of the hemorrhagic group only but it was % in the ischemic group; this was significant (P<.). Good recovery (marked + partial recovery without RT recorded in % of hemorrhagic group but it was % in the ischemic group. The unsafe swallowing group required admission for a longer time (9.) than the safe group (. days) (Table ). From the forty patients included in our study, patients who developed dysphagia in stage I were eliminated in stage II and five patients who developed dysphagia in stage II were eliminated in stage III. Ten patients (%) of the dysphagic group (1) developed chest infection and 1% of patients who had safe swallowing developed chest infection. Chest infection was significantly more common (P<.) among dysphagic group than safe swallowing group (Table ). Out of 19 patients who had no desaturation, no one developed chest infection. Four out of five patients (%) who had >% desaturation, developed chest infection (Table ). Eleven out of thirteen (%) of patients who aspirate (>% desaturation) developed chest infection but only (%) of non aspirated patients (<% desaturation) developed chest infection and this difference is significant statistically (Table ). In Stage 1, the consciousness level (GCS 1), abnormal breathing pattern, weak voice, absent/decreased tongue movements and poor voluntary cough had 1% positive predictive value for predicting chest infection. Impaired gag reflex had sensitivity of 9% and specificity of 9% and low positive predictive value of 1 Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1

3 % but good negative predictive value of % (Table ). In Stage, impaired laryngeal movements and poor voice quality had sensitivity of % and % respectively and 1% specificity and positive predictive value for predicting chest infection. Water dribbling during swallowing had good negative predictive value (9%). 'Poor coughing' had good specificity of %, low positive predictive value (%) but good negative predictive value (%) for development of chest infection (Table ). In Stage, inability to finish ml of aliquots, poor voice quality, and choking on fluids' had higher specificity of 1%-9%-9% and good negative predictive value of %-%-% respectively. Cough in Stage had specificity (%) with poor positive predictive value of %, but had good negative predictive value (9%) in determining the risk of development of chest infection (Table ). SSA test, devised as a bedside tool to predict chest infection, was sensitive enough to predict development of chest infection (%) and had good specificity (%) with positive predictive value of %. Pulse oximetry, which is also a bedside tool has sensitivity of % and a high specificity of 9% with positive predictive value of % and negative predictive value of 91% (Table 9). Table 1. Comparative distribution of dysphagia and resp. morbidity (chest infection), with the laterality of the lesion, stroke (type, site, size) & GCS. Laterality Domin. Non domin. Brain stem Type Hgic Ischemic Cortical Subcortical Brain stem Size Small Moderate Large GCS >1 <1>1 Total Dysphagia Resp. Morb. Patient with Patient without Patient with Patient without No. % No. % No. % No. % No. % * 1 ** * 1 11 * Total number of patients = (F- 1M) Total hgic stroke = [Lobar () thalamic and B.G. () brain stem (1)] Small size = the largest diameter <cm, * Significant <., Moderate size = the largest diameter >-<cm, ** Highly significant <.1, Large size = the largest diameter >cm Table. Chest infection and outcome among the studied patients regarding the swallowing safety and the stroke (type & site). Total Chest Outcome no infection Death Partial recovery with RT feeding Partial recovery without RT feeding Marked recovery Swallowing safety Dysphagia 1 1 *(%) **(%) (%) (9%) (11%) Safe swallowing (1%) 1(%) 1(%) Total 1(.%) (1%) (1.%) 19(.%) 1(%) Stroke Hgic () 1 1 (1%) Ischemic () 1 11*(%) Cortical Subcotrical Brain stem N.B.: RT=Ryle's tube, * Significant <. ** Highly significant <.1 The mean duration of admission was 9. days for dysphagic group and. days for the safe swallowing group 1 1* 1 1 * 1 1 * 1 ** * * ** 9 1 Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1 1

4 Table. Distribution of patients in different stages of SSA and development of chest infection. Morbidity parameters Dysphagia (unsafe swallowing) Safe swallowing Stage I () Chest infection * 11 1 No chest infection Total Stage II () Chest infection 11 No chest infection 1 Total Stage III () Chest infection No chest infection 19 Total 11 Total 1(%) (%) (1%) * Significant <. Total Table. Respiratory morbidity in relation to pulse oximetry results (% of desaturation). Morbidity parameters % of destruction Total % 1% % >% Chest infection 1 (.%) No Chest infection (.%) Total 19 (1%) Table. Respiratory morbidity (chest infection) in relation to swallowing safety and pulse oximetry. Swallowing safety Chest infection No chest infection Total Dysphagia 1* (%) (%) 1 Safe swallowing (1%) 19* (%) Pulse oximetry Total 1 (.%) (.%) Aspirator 11* (%) (1%) 1 Non aspirator (%) * (9%) Total 1 N.B.: Aspirator: patient who had desaturation >% from patient's base line Non aspirator: patient who had desaturation < % from patient's base line * Significant <. 1 Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1

5 Table. Occurrence of respiratory morbidity in different parameters of stage 1 of SSA. Stage 1 parameter Total No. Pt. with resp. morbid Pt. without resp. morb No. % No. % Consc. Level Abnormal <1->1 Normal >1 Head control Abnormal Normal Breathing pattern Abnormal Normal Palatal movement Gag reflex Weak voice Tongue movement /decreased Voluntary cough Lip closure * Significant < * 9 1* 9* * * * Table. Occurrence of respiratory morbidity in different parameters of stage of SSA. Stage parameter Total No. Pt. with resp. morb. Pt. without resp. morb. No. % No. % Water dribbling Laryngeal movement Coughing Choking Voice quality Abnormal normal * Significant < * * * * Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1 19

6 Table. Occurrence of respiratory morbidity in different parameters of stage of SSA. Stage parameter Total No. Pt. with resp. morbid Pt. without resp. morb No. % No. % Unable to finish >1 attempt Coughing Choking Dribbling Voice quality Abnormal normal Table 9. Values of SSA test and pulse oximetry in predicting respiratory morbidity. Sensitivity % Specifity % +ve predictive value % -ve predictive value % SSA test % % % % Pulse oximetry % 9% % 9% DISCUSSION Dysphagia following acute stroke is a common and serious problem. Contrary to earlier belief that brainstem and bicortical involvement only can lead to dysphagia it is being increasingly recognized now that unilateral hemispherical affection can cause dysphagia -. Byrun and Gathier 1 discussed reports of lower precentral gyrus and posterior part of the inferior frontal gyri that caused a cortical form of pseudobulbar palsy with dysphagia, "the operculum syndrome". Of all stroke patients with dysphagia, -% aspirates, % develop chest infections and.% die of pneumonia following stroke -. Dysphagia being an independent marker of post-stroke morbidity and mortality 1,19. Although video fluoroscopy is the gold standard for swallowing assessment, the SSA has been proven to be easier to administer, comparably effective with less risk to patients and with higher negative predictive value as compared to video fluoroscopy. In this study, the level of consciousness was significantly related to dysphagia. Conscious-ness has a major impact on the integrity of the swallowing mechanism. The initial stages of swallowing are controlled by voluntary mechanism governed by facial, tongue and pharyngeal movements which are bound to be affected by altered sensorium. The later stages which are largely involuntary are controlled by subcortical mechanisms which may be affected by basal ganglia, thalamic, large hemispherical or bihemispherical lesions. In this study all patients with GCS<1 and % of alert patients (GCS>1) had swallowing problem. In a study by Ellul et al., in post-stroke patients, % patients with 'drowsy with arousable state' developed dysphagia, whereas only % of alert patients were similarly affected. Similar results were also noted by Barer et al. 1. The laterality of neurological deficit did not appear to influence the development of dysphagia and respiratory morbidity; % of non-dominant hemispherical lobe developed dysphagia, but it was % among dominant hemisphere lesions. However, the impact of dominant lobe affection on dysphagia cannot be commented upon, as the majority of patients 1 Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1

7 had subcortical infarction (1/). Barer 1 has shown the presence of post-stroke dysphagia in % of patients with dominant hemispherical lobe involvement versus % patients with non-dominant hemisphere involvement. It appears that unilateral affection of either lobe, dominant or non-dominant can result in dysphagia, contrary to the earlier belief that only bihemispherical lesions; where supratentorial structures are concerned, could lead to dysphagia 19,. On analysis of the site of infarction with dysphagia, brainstem strokes had the highest incidence (%). But this is non significant statistically; this could be due to very little number patients (1%). Dysphagia is common with brain stem strokes due to lower motor involvement of bulbar swallowing mechanisms and possibility of reticular system involvement. In studies by Horner et al. and De Pippo et al. 9, % and % of brainstem strokes respectively developed dysphagia. Large lesion had 1% propensity to develop dysphagia. It appears to have the worst outcome with respect to both mortality and morbidity; possibly related to large area of hemispherical lesion. The findings are comparable with the study of Ellul et al.. Studying the relation of the size of lesion and final outcome clearly indicates that patients with large size lesion were more morbid, dysphagia being persistent during discharge and recovery being incomplete. The large size lesion group also had % mortality. These findings are comparable to the Ellul et al., study showing 9% mortality and % dependency in TACI (total anterior circulation infarction) patients and % mortality and % dependency in the LACI (lacunar anterior circulation infarction) group. From the results we found that out of patients who had safe swallowing, none expired and none had dependency at discharge, whereas % patients of the 'unsafe swallowing' group either expired or was dependent on discharge. Thus, a significant relation between unsafe swallowing and morbidity, mortality and dependency at discharge could be concluded. Pulse oximetry is a reliable method for the detection of aspiration in dysphagic stroke patients. There is close correlation between aspirations as diagnosed clinically and the drop in arterial blood oxygen saturation (de-saturation) measured by pulse oximetry 1. Aspiration is considered a severe level of dysphagia. All patients with aspiration have dysphagia but not all patients with dysphagia aspirate. Aspirators were found to be at a significantly higher risk of development of chest infection. Pulse oximetry desaturation while swallowing, was a good predictor of subsequent respiratory morbidity in this study with specificity of 9%. These findings were comparable with studies by Debora et al. and Zaidi et al. 1, who also confirmed oxygen desaturation on swallowing as a marker of aspiration in acute stroke. On attempting to fined the relationship of pulse oximetry desaturation with failure of SSA, the following was noted: in Stage, all SSA' failed patients () had desaturation %, and four of them developed chest infection. Seven out of patients who had safe swallowing at stage, developed chest infection eventually, and only / (9%) patients had desaturation by % at this stage. In stage, /11 patients judged to be having unsafe swallowing, developed chest infection. All four patients desaturated by % and / patients judged to be having safe swallowing developed chest infection; out of which one patient desaturated by %. Thus, the seven patients who developed chest infection despite clearing SSA and the three patients who developed chest infection despite clearing SSA, were in reality identified as 'silent aspirators' (doesn't trigger cough or cause symptoms and signs of respiratory distress) on pulse oximetry over and above the SSA. In stage 1 of SSA consciousness level, abnormal breathing pattern, weak voice, decreased tongue movements and poor cough were very specific parameters to indicate the development of dysphagia and chest infection. However, each of these parameters has significantly lower sensitivity, if considered individually. In stage, poor laryngeal movements, abnormal voice and lack of choking were highly specific (1%) and predictive of chest infection (1%), whereas water dribbling had high negative predictive value (9%) for chest infection. In stage, voice quality remains the parameter with fair negative (%) and positive predictive value (PPV) (%). Coughing had better negative predictive value {NPV}(9%). In assessing patients from stage 1 to stage it is evident that the earliest stage had highest PPV and specificity but low sensitivity to predict chest infection. Therefore patients judged to have 'unsafe swallowing' at SSA 1 had 1% chance of developing chest infection, but 'safe swallowing' at SSA 1 did not rule out risk of respiratory morbidity as NPV was lower. The early stages evaluate more obvious and gross abnormalities, as compared to the later stage, where more subtle and discrete dysfunction is assessed. Hence, "failing the earlier stage would have high PPV for predicting respiratory morbidity". Even at the end of stage, / patients who were judged to be safe developed respiratory morbidity. These were possibly 'silent aspirators'. Analyzing the outcome of patients; chest infection and mortality were seen both during the early and intermediate period and were closely related to unsafe swallowing, large lesions, and low GCS. Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1 11

8 Conclusion The presence of large sized lesion or GCS<1 is significantly related with subsequent dysphagia, respiratory morbidity and morality. SSA failure and desaturation >% on pulse oximetry are also significantly related with dysphagia, respiratory morbidity and mortality and dependency status at discharge. REFERENCES 1. Groher ME, Bukatman R. The prevalence of swallowing disorders in two teaching hospitals. Dysphagia. 19;1:1-.. Barer DH. The natural history and functional consequences of dysphagia after hemisphere stroke. J Neurol Neurosurg Psychiatry. 199;:-1.. Wade DT, Langton-Hewer R. Motor loss and swallowing difficulty after stroke: Frequency, recovery and prognosis. Acta Neurol Scand. 19;:-.. Kidd D, Lawson J, Nesbit R, Macmohan J. The natural history and clinical consequences of aspiration following acute stroke. Q J Med. 199;:9-1.. Dantas RO, Kern MK, Massey BT, Dodds WJ, Kahrilas PJ, Brasseur JG, et al. Effect of swallowed bolus variables on oral and pharyngeal phases of swallowing. Am J Physiol. 199; ( Pt 1):G- 1.. Ali GN, Wallace KL, Schwartz R, DeCarle DJ, Zagami AS, Cook IJ. Mechanisms of oralpharyngeal dysphagia in patients with Parkinson's disease. Gastroenterology. 199; 11():-9.. Patten J: Neurological differential diagnosis. London: Harold Starke; 19.. Logemann JA, Kahrilas PJ, Kobara M, Vakil MB. The benefit of head rotation on pharyngeosophageal dysphagia. Arch Phys Med Rehabil. 199; : Meadows JC. Dysphagia in unilateral cerebral lesions: J Neurol Neurosurg Psychiat. 19;:-. 1. Winstein CJ. Neurogenic dysphagia. Phys Ther. 19;: Tuch BE, Nielsen JM. Apraxia of swallowing. Bulletin of Los Angeles Neurological Society. 191; : Veis SL, Logemann JA. Incidence and nature of swallowing disorders in CVA patients. San Francisco: American Speech and Hearing Association; Bruyn GW, Gathier JD. The operculum syndrome. In: Viken PJ, Bruyn GW, editors. Handbook of clinical neurology. Vol. Localisation in clinical neurology. nd ed. Amsterdam: North-Holland Publishing Company; 19. p Barer D. Lower cranial nerve motor function in unilateral vascular lesions of cerebral hemisphere. BMJ. 19; 9: Smithard DG, O'Neill PA, Parks C, Morris J. Complications and outcome after acute stroke: Does dysphagia matter? Stroke. 199; : Horner J, Massey EW, Riski JE, Lathrop DL, Chase KN. Aspiration following stroke: Clinical correlates and outcome. Neurology. 19; : Kalra L, Smith DH, Crome P. Stroke in patients ages over yrs: Outcomes and predictors. Postgrad Med J. 199; 9: Barer DH, Mitchell JR. Predicting the outcome of stroke:do multivariate models help? Q J Med. 199; : Singh S, Hamdy S. Dysphagia in stroke patients. Postgrad Med J. ; : Ellul J, Watkins C, Bared D. The merseyside and North West stroke dysphagia collaboration. frequency, clinical course and complications of dysphagia in acute stroke, studied using a standardised bedside swallowing assessment. Available from: 1. Collins MJ, Bakheit AMO. Does pulse oximetry reliably detect aspiration in dysphagic stroke patients? Stroke. 199; :1-.. Smith HA, Lee SH, O'Neill PA, Connolly MJ. The combination of bedside swallowing assessment and oxygen saturation monitoring of swallowing in acute stroke: A safe and humane screening tool. Age Ageing. ; 9(): Dziewas R, Ritter M, Schilling M, Konrad C, Oelenberg S, Nabavi DG, et al. Pneumonia in acute stroke patients fed by nasogastric tubastric tube. J Neurol Neurosurg Psychiat ; : -.. Martino R, Foley N, Bhogal S, Diamant N, Speechley M, Teasell R. Dysphagia after stroke: Incidence, diagnosis and pulmonary complications. Stroke. ; : -.. Smithard DG, O'Neill PA, Park C, England R, Renwick DS, Wyatt R, et al.; North West Dysphagia Group. Can bedside assessment reliably exclude aspiration following acute stroke? Age Ageing. 199; : Longemann JA. Evaluation and treatment of swallowing disorders. San Diego, CA: College-Hill Press; 19.. Kahrilas PJ. Anatomy, physiology and pathophysiology of dysphagia. Acta Otorhinolaryngol Belg. 199; (): Jennifer Horner. Dysphagia following brainstem stroke. Arch Neurol 1991;: DePippo KL, Holas MA, Reading MJ. The Burke dysphagia screening test: Validation for its use in patients with stroke. Arch Phys Med Rehabil. 199; : Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1

9 . Deborah JCR, David GS, Lailt K. Early assessment of dysphagia and aspiration risk in acute stroke patients. Stroke. ; : Zaidi NH, Smith HA, King SC, Park C, O'Neil PA, Connolly MJ. Oxygen desaturation on swallowing as potential marker of aspiration in acute stroke. Age Ageing. 199; : -. الملخص العربى صعوبة البلع بعد السكتة المخية : التشخيص والمضاعفات pulse oximetry SSA Egypt J Neurol Psychiat Neurosurg. Jan 1 Vol Issue 1 1